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Journal of the American Society of... Aug 1991Post-renal transplant hypertension remains a common problem. The most frequent causes now are chronic rejection and cyclosporine-induced hypertension. Before the... (Review)
Review
Post-renal transplant hypertension remains a common problem. The most frequent causes now are chronic rejection and cyclosporine-induced hypertension. Before the development of cyclosporine, renin-dependent hypertension was the dominant pathophysiological mechanism but now, with the widespread use of cyclosporine, a salt-dependent mechanism is the major one. In severe "inappropriate" hypertension, potentially surgically remediable causes such as renal artery stenosis of the allograft artery or renin release from the native kidneys should be considered. Cyclosporine causes hypertension in normal subjects and in all solid organ transplants. The most likely mechanism is renal vasoconstriction with subtle retention of sodium chloride together with systemic vasoconstriction. The vasoconstriction, as yet, is not associated with any specific vasoconstricting agent nor does there appear to be a specific antagonist. Indeed, increased sensitivity to many different vasoconstrictors has been demonstrated. The major site of vasoconstriction appears to be in the afferent arteriole, and optimum antihypertensive therapy is probably provided by calcium channel blockers if the hypertension is due to cyclosporine. Because post-renal transplant hypertension is often multifactorial in origin, however, it is not surprising that the use of combined antihypertensives is often necessary.
Topics: Antihypertensive Agents; Graft Rejection; Humans; Hypertension, Renal; Kidney Transplantation; Vasoconstriction
PubMed: 1932642
DOI: 10.1681/ASN.V22s37 -
Journal of Clinical Neuroscience :... May 2017We describe the case of a 10-year-old boy who developed reversible cerebral vasoconstriction syndrome (RCVS) after cerebellitis. He received intravenous immunoglobulin...
We describe the case of a 10-year-old boy who developed reversible cerebral vasoconstriction syndrome (RCVS) after cerebellitis. He received intravenous immunoglobulin and methylprednisolone to treat the cerebellitis. However, he then presented with a sudden severe headache, vomiting, and generalized tonic-clonic seizure. Brain magnetic resonance angiography (MRA) initially revealed diffuse cerebral vasodilatations, and diffuse multifocal segmental vasoconstrictions developed several days later. His clinical symptoms gradually resolved after several days, in the absence of any specific therapy. MRA performed 46days after symptom onset showed that the multifocal segmental vasoconstrictions had resolved, suggesting a diagnosis of RCVS. The imaging features of RCVS include multifocal segmental vasoconstriction. However, our case suggests that diffuse cerebral vasodilatation may in fact be evident during the early stage of disease.
Topics: Brain Diseases; Child; Humans; Magnetic Resonance Angiography; Male; Syndrome; Vasoconstriction; Vasodilation
PubMed: 28209305
DOI: 10.1016/j.jocn.2017.01.010 -
Renal Failure Jan 1999The present studies measured vessel diameter, before and after addition of hemolysate, in isolated afferent arterioles (AA) and efferent arterioles (EA) obtained from...
The present studies measured vessel diameter, before and after addition of hemolysate, in isolated afferent arterioles (AA) and efferent arterioles (EA) obtained from the rat kidney. Human red blood cells (RBC) were hemolyzed in distilled water and membranes were discarded after centrifugation. Hemolysate added to the bath solution caused vigorous AA and EA contraction and, after washout, hypersensitized the AA and EA to doses of angiotensin II (AII) which would normally only elicit 50% contraction (EC50). Neither the contraction nor the hypersensitization were mimicked by pure human hemoglobin. The vasoconstrictive responses in the AA and EA were accompanied by increased cytosolic-free calcium concentration. Further purification (desalting) of the hemolysate to remove substance of < or = 1000 Da (which include ATP) did not eliminate the vasoconstrictive component from the hemolysate. Finally, cultured rat aortic vascular smooth muscle cells also demonstrated a rapid increase in (Ca2+i) when exposed to hemolysate. This increase in (Ca2+i) was, in part, dependent on Ca2+ influx since it could be attenuated with diltiazem (10(-5) M). In conclusion, hemolysate contains a factor which induces contractions of the isolated rat kidney AA and EA and rapid elevations in (Ca2+i). This factor, from hemolyzed RBC, is not hemoglobin itself.
Topics: Animals; Aorta; Arterioles; Biological Factors; Calcium; Diltiazem; Erythrocytes; Hemolysis; In Vitro Techniques; Kidney; Muscle, Smooth, Vascular; Rats; Vasoconstriction
PubMed: 10048115
DOI: 10.3109/08860229909066967 -
Journal of Hypertension. Supplement :... Apr 1992To review the effect of damaged endothelium on the development of atherosclerotic disease. (Review)
Review
PURPOSE
To review the effect of damaged endothelium on the development of atherosclerotic disease.
BACKGROUND
Atherosclerotic cardiovascular disease is a complex problem involving lipid deposition, blood pressure, rheologic forces, carbohydrate tolerance and thrombogenic factors. The loss of functional, if not structural, integrity of the vascular endothelium is closely related to the initiation of atherosclerosis. The endothelium contributes to local vascular regulation. Normal endothelial cells are thrombo-resistant; they prevent leukocyte adhesion and control vascular tone by converting angiotensin I into angiotensin II, inactivating bradykinin, norepinephrine, serotonin and ADP, and by secreting vasodilator substances, such as prostacyclin and endothelium-derived relaxing factor (EDRF), and contracting factors such as endothelin. Endothelin is a potent vasoconstrictor peptide that increases intracellular calcium, causing a rapid and transient increase in c-fos and c-myc messenger (m)RNA levels and DNA synthesis in rat vascular smooth muscle cells. In isolated vessel segments, altered endothelial vasoreactivity is usually demonstrated following mechanical trauma to the endothelium.
METHODS AND RESULTS
We investigated the function of normal and damaged endothelium in pigs, following superficial balloon injury, which produces a significant alteration in endothelium-dependent coronary vasoreactivity. The anesthetized pigs were given an intracoronary (left anterior descending artery) infusion of acetylcholine. The balloon injury caused a local transient spasm while the distal uninjured vessel did not change. When acetylcholine was given before the balloon injury, the diameter of the left anterior descending artery did not change, even after preconstriction in vivo with prostaglandin (PG) F2 alpha, but acetylcholine given after the balloon angioplasty caused dose-dependent vasoconstriction. It is known that vasoconstriction in arteries can reduce blood flow and increase arterial wall-shear forces, which increase platelet deposition in injured arteries and may precipitate rupture of atherosclerotic plaques.
CONCLUSION
The intact endothelium is one of the greatest sources of protection from arterial thrombosis, atherosclerosis and vasoconstriction.
Topics: Acetylcholine; Animals; Arteriosclerosis; Bradykinin; Endothelium, Vascular; Swine; Vasoconstriction
PubMed: 1593302
DOI: No ID Found -
Circulation Sep 1988Endothelial injury in vivo is associated with platelet deposition and a localized platelet-dependent vasoconstrictive response. To assess the influence of nitroglycerin...
Endothelial injury in vivo is associated with platelet deposition and a localized platelet-dependent vasoconstrictive response. To assess the influence of nitroglycerin on platelets and vasoconstriction, quantitative 111In-labeled platelet deposition (no platelets x 10(6)/cm2) of the injured segment and the degree of angiographic vasoconstriction (percent diameter narrowing proximal and distal to the dilated segment) produced during injury by balloon angioplasty of the common carotid arteries were studied in heparinized normal pigs that were sacrificed immediately after the procedure. In deeply injured (injury extending through the internal elastic lamina) compared with mildly injured (deendothelialization only) arteries, there was both greater platelet deposition (63.8 vs. 6.9, p = 0.04) and more vasoconstriction (30% vs. 19%, p = 0.02). In the presence of deep arterial wall injury, nitroglycerin given intravenously at a dose sufficient to lower mean arterial pressure by 9 +/- 2% significantly decreased both platelet deposition (16.2 vs. 63.8, p less than 0.008) and the vasoconstrictive response (20 vs. 30%, p less than 0.02) relative to control. However, in the presence of mild arterial wall injury, nitroglycerin decreased vasoconstriction relative to control (10% vs. 19%, p less than 0.01) without causing a significant decrease in the already low level of platelet deposition (5.6 vs. 6.9, respectively; p = NS), suggesting a direct smooth muscle relaxant effect of nitroglycerin. This is the first reported in vivo effectiveness of nitroglycerin in the reduction of platelet deposition after deep arterial injury.
Topics: Angioplasty, Balloon; Animals; Arteries; Blood Platelets; Fibrinolytic Agents; Nitroglycerin; Swine; Vasoconstriction; Wounds, Penetrating
PubMed: 2970342
DOI: 10.1161/01.cir.78.3.712 -
Bioelectromagnetics Feb 2008A variety of medical procedures is aimed to selectively compromise or destroy vascular function. Such procedures include cancer therapies, treatments of cutaneous...
A variety of medical procedures is aimed to selectively compromise or destroy vascular function. Such procedures include cancer therapies, treatments of cutaneous vascular disorders, and temporary hemostasis during surgery. Currently, technologies such as lasers, cryosurgery and radio frequency coagulation, produce significant collateral damage due to the thermal nature of these interactions and corresponding heat exchange with surrounding tissues. We describe a non-thermal method of inducing temporary vasoconstriction and permanent thrombosis using short pulse (microseconds) electrical stimulation. The current density required for vasoconstriction increases with decreasing pulse duration approximately as t(-0.25). The threshold of electroporation has a steeper dependence on pulse duration-exceeding t(-0.5). At pulse durations shorter than 5 micros, damage threshold exceeds the vasoconstriction threshold, thus allowing for temporary hemostasis without direct damage to surrounding tissue. With a pulse repetition rate of 0.1 Hz, vasoconstriction is achieved approximately 1 min after the beginning of treatment in both arteries and veins. Thrombosis occurs at higher electric fields, and its threshold increases with vessel diameter. Histology demonstrated a lack of tissue damage during vasoconstriction, but vascular endothelium was damaged during thrombosis. The temperature increase does not exceed 0.1 degrees C during these treatments.
Topics: Animals; Blood Vessels; Chick Embryo; Dose-Response Relationship, Radiation; Electric Stimulation; Electric Stimulation Therapy; Radiation Dosage; Thrombolytic Therapy; Vasoconstriction
PubMed: 17918191
DOI: 10.1002/bem.20368 -
American Journal of Physiology. Heart... Aug 2001Increases in shear stress promote coronary vasodilation by stimulating the production of nitric oxide (NO). Whether shear stress-induced NO production also limits...
Increases in shear stress promote coronary vasodilation by stimulating the production of nitric oxide (NO). Whether shear stress-induced NO production also limits vasoconstriction in the coronary microcirculation in vivo is unknown. Accordingly, we measured microvascular diameter and flow velocity in the beating heart along with estimated blood viscosity to calculate shear stress during vasoconstriction with endothelin or vasopressin. Measurements were repeated in the presence of NG-monomethyl-L-arginine (L-NMMA) to inhibit NO production and BQ-788 to block NO-linked endothelin type B receptors. BQ-788 did not augment steady-state constriction to endothelin, suggesting that NO production via activation of this receptor is inconsequential. L-NMMA potentiated constriction to both agonists, particularly in small arteries (inner diameter >120 microm). Shear stresses in small arteries were elevated during constriction and further elevated during constriction after L-NMMA. These observations suggest that NO production limits vasoconstriction in the coronary microcirculation and that the principal stimulus for this governance is elevated shear stress. The degree of shear stress moderation of constriction is heterogeneously distributed, with small arteries displaying a higher degree of shear stress regulation than arterioles. These results provide the strongest evidence to date that shear stress-mediated production of NO exerts a "braking" influence on constriction in the coronary microcirculation.
Topics: Animals; Coronary Vessels; Dogs; Enzyme Inhibitors; Nitric Oxide; Oligopeptides; Piperidines; Vasoconstriction; omega-N-Methylarginine
PubMed: 11454584
DOI: 10.1152/ajpheart.2001.281.2.H796 -
Regional Anesthesia 1995
Topics: Anesthesia; Fingers; Humans; Oximetry; Vasoconstriction
PubMed: 8608081
DOI: No ID Found -
Lancet (London, England) Jan 1999The very potent endogenous vasoconstrictor endothelin was discovered in 1988. We know now that there are three isoforms (1, 2, and 3) and two receptor subtypes (A and... (Review)
Review
The very potent endogenous vasoconstrictor endothelin was discovered in 1988. We know now that there are three isoforms (1, 2, and 3) and two receptor subtypes (A and B). A whole range of peptide and non-peptide antagonists has been developed, some selective for A or B receptors and others with non-selective A/B antagonistic activity. So far the main application of these agents has been experimental--ie, endothelin blockers are used to throw light on disease mechanisms, most notably cardiovascular and renal. However, the non-selective antagonist bosentan and a few other agents have been studied clinically. Evidence so far from preclinical studies and healthy volunteers and from the limited number of investigations in patients permits a listing of the potential areas of clinical interest. These are mainly cardiovascular (eg, hypertension, cerebrovascular damage, and possibly heart failure) and renal. Clouds on the horizon are the need to show that these new agents are better than existing drugs; the possibility of conflicting actions if mixed A/B antagonists are used; and animal evidence hinting that endothelin blockade during development could be dangerous.
Topics: Animals; Cardiovascular Diseases; Endothelin Receptor Antagonists; Endothelins; Humans; Receptors, Endothelin; Vasoconstriction
PubMed: 10023915
DOI: 10.1016/S0140-6736(98)09423-9 -
Journal of Clinical Monitoring Jul 1994Thermoregulatory vasoconstriction locally increases arterial wall tension and arteriolar resistance, thereby altering physical properties of the arteries. The arterial...
OBJECTIVE
Thermoregulatory vasoconstriction locally increases arterial wall tension and arteriolar resistance, thereby altering physical properties of the arteries. The arterial pressure waveform is an oscillatory phenomenon related to those physical characteristics; accordingly, we studied the effects of thermoregulatory vasomotion on central and distal arterial pressures, using three hydraulic coupling systems having different dynamic responses.
METHODS
We studied 7 healthy volunteers. Central arterial pressure was measured from the femoral artery and distal pressure was measured from the radial artery, using 10.8-cm long, 20-gauge catheters. Three hydraulic coupling systems were used: (1) a 10-cm-long, 2-mm internal diameter connector; (2) a 150-cm-long, 1-mm internal diameter connector (Combidyn 520-5689, B. Braun, Melsungen, Germany); (3) a 180-cm long, 2-mm internal diameter connector (Medex MX564 and MX562, Medex Inc., Hillard, OH). Brachial artery pressure was measured oscillometrically. Core temperature was measured at the tympanic membrane. The vasomotor index, defined as finger temperature minus room temperature, divided by core temperature minus room temperature, was used to estimate the degree of vasoconstriction. Constriction was considered near maximal when the index was less than 0.1, and minimal when it exceeded 0.75. Measurements were taken every 3 min. Baseline readings were obtained when subjects were warm. They then were cooled by exposure to 20 degrees C to 22 degrees C room air and a circulating-water mattress set at 4 degrees C until index was less than 0.1. They then were rewarmed by increasing water temperature to 42 degrees C and adding a forced-air warmer until the vasomotor index exceeded 0.75. Data were analyzed by ANOVA and linear regression.
RESULTS
Thermoregulatory vasoconstriction was associated with marked arterial pressure waveform changes. Radial pressure showed, in lieu of a dicrotic notch, large oscillations of decreasing amplitude. Femoral pressure showed a single diastolic oscillation of smaller amplitude. The waveforms appeared different, depending on the hydraulic coupling system used, artifact being more marked with the longer connectors. On the average, radial systolic pressure exceeded femoral systolic pressure during vasoconstriction; however, during vasodilatation, femoral systolic pressure exceeded radial systolic pressure (p < 0.05). Oscillometric measurements underestimated systolic pressure, and did so more markedly during vasoconstriction. There were no differences in the values of mean and diastolic pressures.
CONCLUSION
Thermoregulatory vasoconstriction alters radial arterial pressure waveform, artifactually increasing its peak systolic pressure compared with the femoral artery. Poor dynamic responses of recording systems further distort the waveforms. Consequently, radial artery pressure may be misleading in vasoconstricted patients.
Topics: Adult; Blood Pressure; Body Temperature Regulation; Femoral Artery; Humans; Male; Radial Artery; Vasoconstriction
PubMed: 7931452
DOI: 10.1007/BF02899507