Myogenic autoregulation of flow may be inversely related to endothelium-derived relaxing factor activity

Page H1175: T. M. Griffith and D. H. Edwards. “Myogenic autoregulation of flow may be inversely related to endothelium-derived relaxing factor activity.” In Fig. 4, the correct values of conductance are exactly 1/100 smaller than those originally shown. In the second and third line of the left-hand column, the unit of incremental conductance is mmHg–1, not mmHg·min·ml–1.

Effect of aminophylline on hindlimb blood flow autoregulation during increased metabolism in dogs

The contribution of adenosine to hindlimb blood flow autoregulation during treadmill exercise or the administration of 2,4-dinitrophenol (DNP) was evaluated in 9 conscious dogs by determining hindlimb vascular bed pressure-flow relationships in the presence and absence of the adenosine receptor site antagonist, aminophylline. Hindlimb pressure-flow relationships were obtained by measuring blood flow during stepwise reductions in perfusion pressure produced with an occlusion cuff located distal to a flow probe on the external iliac artery. The efficiency of autoregulation was quantitated by calculating the closed-loop gain of flow regulation (Gc) at each pressure decrement utilizing the equation Gc = 1 - (% delta flow/% delta pressure). A Gc of one represents perfect autoregulation of flow, and a Gc of zero is indicative of a rigid system. During exercise, Gc averaged 0.44 +/- 0.07. Aminophylline reduced the Gc during exercise to -0.07 +/- 0.06 (P less than 0.05). During DNP administration, Gc averaged 0.54 +/- 0.09 and declined to -0.09 +/- 0.10 in the presence of aminophylline (P less than 0.05). These results support the hypothesis that adenosine is a primary mediator of hindlimb blood flow autoregulation during conditions that increase hindlimb metabolism.

Tissue pressure and autoregulation in the dextran-perfused kidney

Experiments were performed on isolated dog kidneys alternately perfused with homologous blood and dextran. Renal artery pressure, tissue pressure, perfusate flow rate and vascular volume changes were measured as arterial pressures were progressively elevated. Marked increases in overall vascular resistance RA/F occurred in all dextran- and blood-perfused kidneys throughout the autoregulatory range. Results indicate that autoregulation of flow occurs in both blood- and dextran-perfused kidneys concurrent with increases in tissue pressure. Dextran- and blood-perfused kidneys show similar degrees of autoregulation when values are expressed in terms of increase in flow per unit rise of arterial pressure and compared to preautoregulation values.

Autoregulation of flow in isolated rat kidney in the absence of red cells

A method was devised for the perfusion of isolated rat kidney without interruption of flow. The flow pattern obtained with cell-free dextran at a constant pressure showed a stable period of maximal flow for about 15–30 minutes. Thereafter the flow resistance of the kidney increased continuously. Autoregulation was maximal during the period of maximal flow, but thereafter deteriorated until it disappeared completely. The autoregulation was diminished by Priscoline and completely but reversibly abolished by procaine. It was concluded that autoregulation involves a physiological rather than a ‘cell separation’ mechanism.