title: Hypertension from carotid occlusion decreases renal papillary plasma flow, hypotension from hemorrhage increases it, an autoregulatory paradox.
abstract: Renal papillary plasma flow was tested during acute increases and decreases of perfusion pressure using the 125I-labelled albumin technique. Increases of pressure were attained through ligation of carotid arteries; decreases of pressure through modest hemorrhage. In 12 control rats with blood pressure of 144 mmHg, the papillary plasma flow averaged 21.5 ml per 100 g papilla per min. In 12 rats after ligation of carotid arteries, blood pressure rose from 143 mmHg to 172, a 20% increase. The papillary plasma flow in these rats with acute hypertension averaged 17.9 ml per 100 g papilla per min, a 17% decrease (p < 0.025). In another 12 rats after bleeding 1% of body weight over a period of 10 min, blood pressure dropped from 146 mmHg to 104, a 29% decrease. The papillary plasma flow in these rats with acute hypotension averaged 26.0 ml per 100g papilla per min, a 21% increase (p < 0.025). The decrease in papillary plasma flow during acute hypertension strongly suggests an increased vascular resistance of the descending vasa recta, while the increase in papillary plasma flow during acute hypotension suggests that vasodilatation occurred in these vessels. This dilatation may be produced by the local release of prostaglandins or other vasoactive substances. Thus, the renal papilla appears to "overshoot" its autoregulation of plasma flow, with actual reduced flow during an acute blood pressure rise and increased flow during an acute blood pressure fall, an enigmatic over-compensation.
authors.affiliation: Renal and Hypertension Section, University of Minnesota Hospital and School of Medicine, Minneapolis 55455, USA.
authors.forename: M
authors.initials: M
authors.lastname: Ganguli
authors.forename: L
authors.initials: L
authors.lastname: Tobian
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D016893:Carotid Stenosis / Q000150:complications / Q000503:physiopathology*; D006400:Hematocrit; D006470:Hemorrhage / Q000150:complications / Q000503:physiopathology*; D006706:Homeostasis / Q000502:physiology*; D006973:Hypertension / Q000209:etiology / Q000503:physiopathology*; D007022:Hypotension / Q000209:etiology / Q000503:physiopathology*; D007679:Kidney Medulla / Q000098:blood supply*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D012079:Renal Circulation / Q000502:physiology; D012964:Sodium / Q000378:metabolism; D014508:Urea / Q000378:metabolism; D014655:Vascular Resistance / Q000502:physiology
chemical_list: D014508:Urea; D012964:Sodium