Vasodilators inhibit acute alpha 1-adrenergic receptor-induced trophic responses in the vasculature.
- 1 December 1992
- journal article
- abstracts
- Published by Wolters Kluwer Health in Hypertension
- Vol. 20 (6), 809-815
- https://doi.org/10.1161/01.hyp.20.6.809
Abstract
Cardiovascular hypertrophy plays an important role in the development and maintenance of hypertension. Hyperactivity of the sympathetic nervous system may be one of the initiating factors responsible for the stimulation of growth processes involved in these structural alterations. We have used a well-established early biochemical marker of cellular growth processes, induction of ornithine decarboxylase (ODC), to determine whether alpha 1-adrenergic receptor-induced vascular trophic responses are dependent on arterial pressure elevation. Hydralazine or felodipine were coadministered to control the alpha 1-adrenergic receptor agonist-induced rise in mean arterial pressure (MAP). Methoxamine (2, 5, or 10 mg/kg s.c.) increased the average MAP (up to 20 mm Hg) and vascular ODC activity (up to ninefold) above control rats over 4 hours. Concomitant administration of hydralazine (0.5, 1.25, or 5 mg/kg s.c.) or felodipine (100 or 250 micrograms/kg s.c.) with methoxamine (10 mg/kg) attenuated the alpha 1-adrenergic receptor-induced activation of ODC in the aorta and mesenteric resistance vasculature, as well as the MAP increases. Vasodilators alone did not lower basal vascular ODC activity. The major findings include: 1) alpha 1-adrenergic receptor activation dose-dependently induces vascular ODC activity concomitantly with MAP elevation, 2) vasodilators inhibited both the alpha 1-adrenergic receptor-induced MAP increases and the activation of mesenteric vascular and aortic ODC, and 3) the stimulus-response correlation between MAP elevation and mesenteric (r = 0.78) and aortic (r = 0.92) ODC activation was characterized by a logistic function.(ABSTRACT TRUNCATED AT 250 WORDS)Keywords
This publication has 20 references indexed in Scilit:
- Angiotensin II causes vascular hypertrophy in part by a non-pressor mechanism.Hypertension, 1991
- Differential development of vascular and cardiac hypertrophy in genetic hypertension. Relation to sympathetic function.Hypertension, 1989
- TIME COURSE OF CHANGES IN BARORECEPTOR REFLEX CONTROL OF HEART RATE IN CONSCIOUS SHR AND WKY: CONTRIBUTION OF THE CARDIAC VAGUS AND SYMPATHETIC NERVESClinical and Experimental Pharmacology and Physiology, 1988
- Structural and functional consequence of neonatal sympathectomy on the blood vessels of spontaneously hypertensive rats.Hypertension, 1987
- Interaction of alpha and beta adrenergic stimulation on aortic ornithine decarboxylase activityLife Sciences, 1985
- Studies of hypertension-induced vascular hypertrophy in cultured smooth muscle cells from spontaneously hypertensive rats.Hypertension, 1983
- Hypertension and cardiovascular hypertrophy during chronic catecholamine infusion in ratsLife Sciences, 1983
- Effect of stress and sympathetic activity on rat cardiac and aortic ornithine decarboxylase activityLife Sciences, 1979
- Background of Increased Flow Resistance and Vascular Reactivity in Spontaneously Hypertensive RatsActa Physiologica Scandinavica, 1970
- Adaptive Structural Changes of the Vascular Walls in Hypertension and their Relation to the Control of the Peripheral Resistance.Acta Physiologica Scandinavica, 1958