title: Hemodynamic and functional changes during renal venous stasis in dog kidneys.
abstract: The effect of renal venous pressure (RVP) elevation on renal hemodynamics and tubular function was studied in neurolept anaesthetized dogs. Renal blood flow (RBF) was measured electromagnetically. Clearance of 51Cr-EDTA was used as a measure of the rate of glomerular filtration (GFR). GFR, urinary excretion rates of sodium and water, and lithium clearance (CLi) were used for assessing the absolute and fractional reabsorption rates of sodium and water in the proximal as well as in more distal segments of the nephron. The vasoconstrictor response to RVP elevation was partly abolished by acute surgical denervation or by local application of lidocain on the renal capsule, suggesting that RVP elevation activates an adrenergic vasoconstrictor reflex comprising the spinal cord, and elicited from stretch receptors located in the renal capsule. Further studies in alpha-adrenoceptor blocked or chronic denervated kidneys and in decapsulated kidneys favour the view, that neurogenic and myogenic mechanisms significantly influence the vasoconstrictor response to RVP elevation: The neurogenic contribution to the vasoconstrictor response comprising intrarenal and extrarenal vasoconstrictor mechanisms evoked reflexly by RVP elevation; the myogenic contribution to the vasoconstrictor response comprising opposing vasodilator mechanisms due to increase in renal interstitial tissue pressure during RVP elevation. Studies carried out in intact kidneys, acutely surgically or chronically denervated kidneys or alpha-adrenoceptor blocked kidneys indicate that the increase in proximal reabsorption rates during moderate RVP elevation is due mainly to local intrarenal alpha-adrenergic reflex mechanisms, since the decrease in CLi (during constant filtered load) induced by RVP elevation was unaffected by acute surgical denervation, but completely abolished by chronic denervation of the kidney, or by local alpha-adrenoceptor blockade of the kidney.
authors.affiliation: Department of Cardiology, Gentofte Hospital.
authors.forename: U
authors.initials: U
authors.lastname: Abildgaard
mesh_terms: D000818:Animals; D003714:Denervation; D004231:Diuresis; D004285:Dogs; D005260:Female; D005919:Glomerular Filtration Rate; D007668:Kidney / Q000294:innervation* / Q000502:physiology; D007684:Kidney Tubules / Q000502:physiology*; D008297:Male; D009318:Natriuresis; D009407:Nerve Block; D010646:Phentolamine / Q000494:pharmacology; D011945:Receptors, Angiotensin / Q000187:drug effects; D012079:Renal Circulation / Q000187:drug effects; D012082:Renal Veins / Q000502:physiology*; D014690:Venous Pressure
chemical_list: D011945:Receptors, Angiotensin; D010646:Phentolamine