In vitro response of rat renal artery to perfusion pressure.
Both tubuloglomerular feedback and a myogenic response contribute to autoregulation of renal blood flow. Vascular interaction initiated by tubuloglomerular feedback has been described and prevents definition, in vivo, of the contribution of myogenic responses to autoregulation. Segments of rat renal artery were perfused in vitro at constant flow while upstream and downstream pressures were measured on-line, allowing determination of resistance. Transmural pressure was governed by a downstream resistor. Outside diameter was measured by an ocular micrometer. The segments were bathed in bicarbonate Ringer solution and perfused with Ringer containing 50 g/L bovine serum albumin. Potassium depolarization reduced the diameter and made it more sensitive to perfusion pressure. Serosal norepinephrine, 10(-7)-10(-5) M, caused graded constriction and increased the axial pressure drop due to vessel resistance. Addition to the perfusate of rat red blood cells to hematocrit approximately 33% significantly reduced arterial diameter and enhanced the increased axial pressure drop induced by 10(-6) M norepinephrine. Sequential elevation of perfusion pressure from 50 to 100 mmHg (1 mmHg = 133.3 Pa) increased the diameter significantly. Red cells reduced the slope of the diameter-pressure relationship. In another experiment, norepinephrine reduced the slope of diameter versus perfusion pressure, while 10(-4) M papaverine plus norepinephrine increased the slope, compared with norepinephrine alone. Norepinephrine caused a sizable axial pressure drop (15.7 +/- 3.7 mmHg), which decayed as perfusion pressure increased; the decay was accentuated by papaverine. The changes in axial pressure drop were linearly related to the inverse 4th power of diameter, indicating that both measurements assessed the same behavior. Several different maneuvers thus affect the relationship between arterial diameter and perfusion pressure, and the relationship between axial pressure drop and perfusion pressure. The results indicate the presence of a myogenic response, which is, however, not strong enough to defend vessel diameter when pressure rises.
Ajikobi
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Department of Medicine, Sir Mortimer B. Davis-Jewish General Hospital, Cóte Ste-Catherine, Montréal, QC, Canada.
Cupples
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D000818:Animals; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D004912:Erythrocytes / Q000502:physiology; D066298:In Vitro Techniques; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology*; D009638:Norepinephrine / Q000494:pharmacology; D010208:Papaverine / Q000494:pharmacology; D010477:Perfusion; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D012077:Renal Artery / Q000033:anatomy & histology / Q000187:drug effects / Q000502:physiology*; D012079:Renal Circulation / Q000502:physiology*
D010208:Papaverine; D011188:Potassium; D009638:Norepinephrine