Role of cardiopulmonary mechanoreceptors in the postural regulation of renin

Abstract

To change the stretch on cardiopulmonary mechanoreceptors, large shifts of blood in the capacity space were elicited by tilting and by exerting positive lower body pressure in the tilted position. Twelve volunteers underwent invasive hemodynamic studies and in 10 other subjects cardiac size was determined by radionuclide cardiography. In all 22 subjects tilting caused the expected increase of renin, which was abolished by lower body compression. Decompression caused renin to increase again. Right atrial pressure in invasive studies and end-systolic and end-diastolic counts in noninvasive studies showed a significant and strong negative correlation with renin and norepinephrine levels. Thus, the degree of stretch of the cardiopulmonary mechanoreceptors is a major determinant of reflex regulation of renin release in humans.

Atrial Natriuretic Factor in Human Pathophysiology

“…increased stretch of atria can, under some circumstances, lead to suppression of renal sympathetic toneandrenin secretion (Linden 1979;Sanchez et al 1987), yet in heart failure this inhibitoryeffect must be overcome by the combined factors noted above. Further, any inhibitory action of ANF itself on the juxtaglomerular apparatus and the adrenal glomerulosa is apparently overcome.…”

“…The likely explanation for this discrepancy is that input stimuli to the juxtaglonierular apparatus in heart failure (increased sympathetic stimulation, decreased renal artery perfusion pressure, reduced chloride and sodium delivery to the macula densa) are akin to those associated with volume depletion in normal man, yet atrial stretch releases ANF in heart failure and decreased stretch inhibits release in volume-depleted normals. In other words, the juxtaglonierular apparatus in heart failure perceives a state of reduced arterial volume whereas the ANF releasing increased stretch of atria can, under some circumstances, lead to suppression of renal sympathetic toneandrenin secretion (Linden 1979;Sanchez et al 1987), yet in heart failure this inhibitoryeffect must be overcome by the combined factors noted above. Further, any inhibitory action of ANF itself on the juxtaglomerular apparatus and the adrenal glomerulosa is apparently overcome.…”

Pneumatic antishock garment inflation activates the human sympathetic nervous system by abdominal compression

“…Also, PASG inflation reduces vascular compliance, thus increasing cardiac afterload and systemic vascular resistance (Gaffney et al 1981; Julius et al 1982; McSwain, 1988; Rubal et al 1989). Prolonged PASG inflation causes predictable humoral events, reducing renin and antidiuretic hormone and increasing atrial natriuretic factor (Hesse et al 1978; Sanchez et al 1987; Geelen et al 1989, 1992; Guezennec et al 1989; Pan et al 1997).…”

“…The sympathetic response to PASG inflation has not been defined clearly. Plasma noradrenaline levels have been reported to decrease during PASG inflation, suggesting baroreflex‐mediated sympathoinhibition in response to the mechanical effects of PASG (Hesse et al 1978; Sanchez et al 1987; Geelen et al 1992; Pan et al 1997). In contrast, animal experiments have identified an increase in noradrenaline in response to PASG inflation (Julius et al 1982).…”