Properties of intestinal and cutaneous arteries and veins in two-kidney one-clip Goldblatt hypertension.
This study evaluates whether changes in arterial and venous smooth muscle contractility and extensibility precede or result from the elevated arterial pressure (MAP) and total peripheral resistance (TPR) of two-kidney one-clip Goldblatt hypertension (2-KGH). The experiments measure the contractile and extensibility properties of rings of canine mesenteric, cutaneous, gracilis, and pulmonary arteries and veins (0.4-1.0 mm OD) prior to and days 1 and 32 after the initiation of two-kidney one-clip Goldblatt hypertension (2-KGH), produced by unilateral constriction of the renal artery (URAC). The reactivity (ED50) and tension development to norepinephrine (NE), angiotensin II (ANG II), potassium chloride (KCl), serotonin (5-HT), 9 alpha, 11 alpha-epoxymethano prostaglandin H2 (EMP), prostaglandin B2 (PGB2), and CaCl2 were determined. Mean arterial pressure (MAP) and TPR were unchanged from pre-URAC values 24 h post-URAC but were significantly elevated 32 days post-URAC. The ED50's for 5-HT, ANG II, EMP, and PGB2 were decreased in each of the arteries and veins obtained from dogs with 2-KGH, within 24 h post-URAC, and either became more pronounced (PGB2, EMP, and 5-HT) or returned to pre-URAC values by day 32 post-URAC. The ED50's for NE, KCl, and CaCl2 were unchanged from pre-URAC values. Maximal tension development of the arteries and veins to each of the agonists increased within 24 h post-URAC, prior to an increase in MAP or TRP. Within 32 days post-URAC, maximal tension development of the veins obtained from 2-KGH was increased from pre-URAC values, whereas tension development by the arteries was decreased. Extensibility decreased in each of the arteries and veins obtained from dogs with 2-KGH 24 h post-URAC. The extensibility decreased further by day 32 post-URAC as the level of MAP and TPR increased. These data support the postulate that altered venous and arterial smooth muscle contractility and extensibility precede the elevated MAP and TPR of 2-KGH in dogs. Moreover, since these changes occur in both artery and vein, they must reflect the action of circulating humoral or intrinsic vascular or neural substances. Finally, the decrease in arterial contractility suggests that the enhanced vascular responses in vivo and in situ may reflect the greater mechanical advantage of the hypertrophied blood vessel and not an arterial vasculature with enhanced contractility.
D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001158:Arteries / Q000502:physiology; D001794:Blood Pressure; D002118:Calcium / Q000494:pharmacology; D004285:Dogs; D005260:Female; D006977:Hypertension, Renal / Q000503:physiopathology*; D008297:Male; D009119:Muscle Contraction; D009131:Muscle, Smooth, Vascular / Q000502:physiology*; D009638:Norepinephrine / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology; D012701:Serotonin / Q000494:pharmacology; D014655:Vascular Resistance; D014680:Veins / Q000502:physiology
D000804:Angiotensin II; D012701:Serotonin; D011188:Potassium; D002118:Calcium; D009638:Norepinephrine