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Venous capacity and compliance in hypertensive adults: influence of hypoxia and hyperoxia.
J Appl Physiol (1985)
June 2023
Department of Physiology, Faculty of Medical & Health Sciences, Manaaki Manawa-The Centre for Heart Research, University of Auckland, Auckland, New Zealand.
In hypertension, the cardiorespiratory responses to peripheral chemoreflex activation (hypoxia) and inactivation (hyperoxia) are reportedly augmented, but the impact on peripheral venous function is unknown. We tested the hypothesis that in hypertensives, both hypoxia and hyperoxia evoke more pronounced changes in lower limb venous capacity and compliance, than in age-matched normotensives. In 10 hypertensive [HTN: 7 women; age: 71.
View Article and Find Full Text PDFSplanchnic circulation is a critical neural target in angiotensin II salt hypertension in rats.
Hypertension
September 2007
Department of Pharmacology and Toxicology, Michigan State University, East Lansing, MI 48824, USA.
Chronic angiotensin II (Ang II) infusion, in rats fed high salt, engages the sympathetic nervous system to increase venomotor tone. The splanchnic sympathetic nervous system is the most important regulator of venous tone, indicating that splanchnic sympathetic nervous system activity may be increased in Ang II salt hypertension. We hypothesized that celiac ganglionectomy (CGx), to selectively disrupt sympathetic innervation to the splanchnic circulation, would attenuate arterial pressure (AP), and venous tone increases in Ang II salt hypertension.
View Article and Find Full Text PDFIncreased sympathetic venoconstriction and reactivity to norepinephrine in mesenteric veins in anesthetized DOCA-salt hypertensive rats.
Am J Physiol Heart Circ Physiol
July 2007
Department of Pharmacology & Toxicology, Neuroscience Program, Michigan State University, East Lansing, MI 48824, USA.
Increased sympathetic nervous activity (SNA) elevates venomotor tone in deoxycorticosterone acetate (DOCA)-salt hypertension. We studied the mechanisms by which the SNA increases venomotor tone in DOCA-salt hypertension by making in situ intracellular recordings of venous smooth muscle cell (VSMC) membrane potential (E(m)) and measurement of outside diameter (OD) in mesenteric veins (MV) and mesenteric arteries (MA) of anesthetized rats. We also studied norepinephrine (NE)- and endothelin-1 (ET-1)-induced increases in MA or MV perfusion pressure (PP) in vitro.
View Article and Find Full Text PDFChronic low-dose angiotensin II infusion increases venomotor tone by neurogenic mechanisms.
Hypertension
November 2006
Department of Pharmacology and Toxicology, Michigan State University, East Lansing, MI 48824, USA.
The purpose of this study was to identify changes in venomotor tone in the chronic low-dose angiotensin II (Ang II) model of hypertension and to establish the contribution of sympathetic nerve activation to these venomotor tone changes. Male Sprague-Dawley rats were acclimatized to a 0.4% or 2.
View Article and Find Full Text PDFMechanisms of hypertension induced by nitric oxide (NO) deficiency: focus on venous function.
J Cardiovasc Pharmacol
June 2006
Department of Pharmacology and Toxicology, Michigan State University, East Lansing, MI 48824-1317, USA.
Loss of endothelial cell-derived nitric oxide (NO) in hypertension is a hallmark of arterial dysfunction. Experimental hypertension created by the removal of NO, however, involves mechanisms in addition to decreased arterial vasodilator activity. These include augmented endothelin-1 (ET-1) release, increased sympathetic nervous system activity, and elevated tissue oxidative stress.
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