SECRETION OF MEDULLIPIN I BY ISOLATED KIDNEYS PERFUSED UNDER ELEVATED PRESSURE
| Autor: | P. Brown, E E Muirhead, B. Brooks, Byers Lw, James A. Pitcock |
|---|---|
| Rok vydání: | 1991 |
| Předmět: |
Male
Leukotrienes medicine.medical_specialty Physiology Urinary system Polysorbates Hemodynamics Blood Pressure In Vitro Techniques Biology Kidney Renal Artery Physiology (medical) Internal medicine medicine.artery Renin–angiotensin system medicine Animals Renal artery Pharmacology Angiotensin II Proadifen Rats Inbred Strains Lipid Metabolism Lipids Medullipin Rats Perfusion Hypertension Renovascular Endocrinology Blood pressure medicine.anatomical_structure Prostaglandins |
| Zdroj: | Clinical and Experimental Pharmacology and Physiology. 18:409-417 |
| ISSN: | 1440-1681 0305-1870 |
| DOI: | 10.1111/j.1440-1681.1991.tb01472.x |
| Popis: | SUMMARY 1. Medullipin I (Med I) is a hormone extracted from renal papillae and its renomedullary interstitial cells (RIC). Med I is stimulated by elevation of the renal artery perfusion pressure. 2. When isolated normal rat kidneys were perfused either with oxygenated blood or with 5% albumin bubbled with O2 at elevated perfusion pressures, Med I appeared to be secreted into the renal venous effluent (RVE). Addition of Tween 20, treatment of the assay rat with SKF 525A, inhibitor of cytochrome P-450 and removal of the liver from the systemic circulation prevented vasodepression of both the RVE and extracted Med I. The lipid in the RVE gave the same dose–response as extracted Med I. 3. Lowering the renal artery perfusion pressure below normal inhibited the secretion of Med I. As the perfusion pressure was elevated Med I secretion appeared to increase. 4. Previous observations and the present study support the view that the renin–angiotensin system and the Medullipin system are double feedback systems involved in blood pressure control. |
| Databáze: | OpenAIRE |
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