The Role of the Macula Densa in Renin Synthesis

Morgan, Trefor; Barrett, Graham L.; Zhang, Yanling; Alcorn, Daine

doi:10.1111/j.1440-1681.1991.tb01421.x

Cited by 4 publications

(1 citation statement)

References 13 publications

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“…Thus, in mice and rats with one hydronephrotic, nonfiltering kidney with severe tubular atrophy, the renal renin mRNA and protein levels were normally regulated in the filtering and nonfiltering kidneys by high and low salt diets [83,107,126,128]. Interestingly however, the renin release from the hydronephrotic kidney did not change in parallel to the renin synthesis, as was the case in the healthy contralateral kidney [127,128]; this result indicated that the macula densa might play a role in the proper renin release in this situation.…”

Section: The Macula Densa Mechanismmentioning

confidence: 94%

Salt feedback on the renin-angiotensin-aldosterone system

Schweda

2014

Pflugers Arch - Eur J Physiol

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The renin-angiotensin-aldosterone system (RAAS) is a central element in the control of the salt and water balance of the body and arterial blood pressure. The activity of the RAAS is controlled by the protease renin, which is released from renal juxtaglomerular epithelioid cells (JGE cells) into the circulation. Renin release is regulated by a complex interplay of several locally acting hormones or mechanisms and longer feedback loops one of which involves salt intake. Acute NaCl loads or longer lasting high salt intakes suppress plasma renin activity, whereas reductions in NaCl intake stimulate it. Because the activation of the RAAS conserves the salt content of the body, a classical feedback loop between salt intake/body salt content and renin is established. Despite of its important role for body fluid homeostasis, the precise signaling pathways connecting salt intake with the synthesis and release of renin are only incompletely understood. Four putative controllers of the salt-dependent regulation of the RAAS have been suggested: (1) the macula densa mechanism which adjusts renin release in response to changes in the renal tubular salt concentration; (2) salt-dependent changes in the arterial blood pressure; (3) circulating salt-dependent hormones, particularly the atrial natriuretic peptide (ANP); and (4) renal sympathetic nervous activity, which is regulated by extracellular volume and arterial blood pressure. In this review, the role of these known controllers of the RAAS will be discussed with special emphasis on their relative contributions to the salt-dependent regulation of the RAAS at different time frames.

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