title: Venous reactivity in canine renovascular hypertension.
abstract: The responsiveness of arterial smooth muscle to vasoactive stimuli is enhanced hypertension. It is however, unclear whether this increased reactivity is a generalised property of vascular smooth muscle, involving veins as well. We examined the responses of rings of cephalic vein in vitro taken from 11 dogs with chronic renovascular hypertension and 10 normal dogs. Mean blood pressure was 129 +/- 3 mmHg in the hypertensive dogs, 26% above control. Veins from hypertensive dogs had steeper passive circumference-tension relationships than veins from normal dogs, indicating reduced compliance. Sensitivity (defined as location of EC50) to potassium depolarisation was unchanged, but maximal contractile force (Fmax) developed was 35% greater in hypertension when compared with normotensive dogs. With noradrenaline and the selective alpha 1-adrenoceptor agonist methoxamine, there was no difference between normotensive and hypertensive dogs in either location of the EC50 or in the Fmax. With the selective alpha 2-adrenoceptor agonist UK 14304, there was a tenfold decrease in sensitivity in hypertension when compared with normotensive dogs, but no change in Fmax. There was, however a tenfold increase in sensitivity to serotonin in hypertension when compared to normotensive dogs, and a 22% increase in Fmax. Contractile responses to transmural sympathetic nerve stimulation were similar in the two groups. As desipramine caused equal increases in responses to neural stimulation, there was no demonstrable abnormality of neuronal uptake in hypertension. Morphometric examination showed no change in media thickness, media thickness/radius ratios or media cross sectional area in hypertension. Therefore, veins from dogs with chronic renovascular hypertension are stiffer but not hypertrophied, and exhibit some specific differences in contractile responses to vasoconstrictor agents when compared with veins from normotensive dogs.
authors.affiliation: Baker Medical Research Institute, Prahran, Victoria, Australia.
authors.forename: K
authors.initials: K
authors.lastname: Sudhir
authors.forename: J J
authors.initials: JJ
authors.lastname: Smolich
authors.forename: J A
authors.initials: JA
authors.lastname: Angus
mesh_terms: D000818:Animals; D001794:Blood Pressure; D004285:Dogs; D004558:Electric Stimulation; D005260:Female; D006225:Hand; D006978:Hypertension, Renovascular / Q000378:metabolism / Q000503:physiopathology*; D066298:In Vitro Techniques; D008297:Male; D009132:Muscles / Q000098:blood supply; D012146:Rest; D014655:Vascular Resistance; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014680:Veins / Q000378:metabolism / Q000503:physiopathology*
chemical_list: D014662:Vasoconstrictor Agents