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J Hypertens Suppl. 1993 Dec;11(5):S53-8.

Renal vasodepressor mechanisms: the medullipin system.

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Department of Pathology, University of Tennessee, Memphis 38163.

Erratum in

  • J Hypertens Suppl 1994 Apr;12(4):following H14.


Renal vasodepressor hormone: Medullipin I is the renomedullary vasodepressor hormone secreted by the renomedullary interstitial cells of the renal papilla. It is conveyed to the liver where it is converted to its active form, medullipin II. Medullipin II is a vasodilator that suppresses sympathetic tone and causes diuresis and natriuresis. Its actions are opposite to those of angiotensin II. These are feedback control systems. The secretion and conversion of medullipin is related to the cytochrome P-450 dependent enzyme system of kidney and liver. Deficiency of medullipin: A deficiency of medullipin is considered to contribute to the pathogenesis of various hypertensive states. There are three known causes for such a deficiency, (1) removal of renomedullary interstitial cells by bilateral nephrectomy, renal surgical papillectomy, chemical papillectomy, papillary atrophy or necrosis; (2) decrease in number and damage to renomedullary interstitial cells in accelerated experimental hypertension and malignant hypertension of humans; and (3) dysfunction of renomedullary interstitial cells as mediated by angiotensin II, by resetting of the effect of increased renal artery perfusion pressure, by stimulation of the renal sympathetic nerve, by inhibition of nitric oxide synthesis and possibly by inhibition of cyclo-oxygenase. Secretion of Medullipin I: The main factor influencing secretion of medullipin I by the kidney appears to be the renal artery perfusion pressure. Elevation of this pressure is attenuated by the presence of medullipin I in the renal venous effluent. Lowering the pressure below normal shuts off this secretion. This is opposite to the effects of perfusion pressure on renin secretion, as elevation shuts off renin secretion while depression turns it on.(ABSTRACT TRUNCATED AT 250 WORDS).

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