Renin response to stimulation of cardiopulmonary mechanoreceptors in man.

Physiology of Vasopressin Relevant to Management of Septic Shock

“…Accordingly, a fall in central venous pressure evokes an increase in norepinephrine and renin, while vasopressin does not increase until mean arterial pressure falls. [31][32][33][34][35] Conversely, volume expansion and large increases in BP transiently inhibit vasopressin release, due more to atrial stretch receptors than to arterial baroreceptors. 36 Hormonal Regulation: Other nonosmotic stimuli that are relevant in critical illness and septic shock include hormones and mediators that directly stimulate vasopressin release, such as acetylcholine (via nicotinic receptors), histamine, nicotine, dopamine, prostaglandins, angiotensin II, and other catecholamines.…”

Role of cardiovascular receptors on the neural regulation of renin release in normal men.

“…Plasma renin activity was assessed by radioimmunoasssay, and plasma norepinephrine concentration by a radioenzymatic assay. 3 …”

“…In addition to data obtained with this predominantly carotid receptor stimulus, information was obtained during supine thigh cuff inflation, which unloads low-pressure receptors by decreasing right atrial pressure and central blood volume without significantly altering arterial pressures. 3 Subjects were placed in the supine position and an 18-gauge 2-inch Teflon catheter was introduced into the left brachial artery, and a 4-French Swan-Ganz catheter or polyethylene 50 catheter was introduced via the left basilic vein into the right atrium. Catheter position was verified by obtaining a characteristic right ventricular tracing and withdrawing the catheter to obtain a right atrial waveform.…”

“…Much of the disagreement centers on the anatomic location of the afferent sensor. The question is whether an increase in renin release in normal humans can occur with unloading (decreased stretch) of either arterial high-pressure 2 or cardiopulmonary low-pressure receptors, 3 or if it is necessary that both receptor systems are simultaneously unloaded.4 There are at least three reasons for obtaining accurate information on this question: 1) understanding factors regulating an important hormone in Received December 6, 1982; revision accepted May 27, 1983. volume and pressure homeostasis is of basic physiological significance; 5 2) our understanding of abnormal renin responses in many patients with hypertension would be improved and this would possibly provide clues regarding the pathophysiology of abnormal responses; and 3) knowing the normal hemodynamic determinants that regulate the function of high-and low-pressure receptors with renin release as an easily measured humoral marker may facilitate research in various disease states where abnormalities of these receptors are suspected. Therefore, we designed the following series of experiments to evaluate the effect on renin release of separate and combined unloading of arterial high-pressure and cardiopulmonary low-pressure receptors.…”

“…Much of the disagreement centers on the anatomic location of the afferent sensor. The question is whether an increase in renin release in normal humans can occur with unloading (decreased stretch) of either arterial high-pressure 2 or cardiopulmonary low-pressure receptors, 3 or if it is necessary that both receptor systems are simultaneously unloaded.…”