Control Of Renal Blood Flow Research Articles

Participation of the prostaglandins in the control of renal blood flow during acute reduction of cardiac output in the dog.

To determine whether renal prostaglandins participate in the regulation of renal blood flow during acute reduction of cardiac output, cardiac venous return was decreased in 17 anesthetized dogs by inflating a balloon placed in the thoracic inferior vena cava. This maneuver decreased cardiac output from 3.69+/-0.09 liters/min (mean+/-SEM) to 2.15+/-0.19 liters/min (P < 0.01) and the mean arterial blood pressure from 132+/-4 to 111+/-5 mm Hg (P < 0.01) and increased total peripheral vascular resistance from 37.6+/-2.5 to 57.9+/-4.8 arbitrary resistance units (RU) (P < 0.01). In marked contrast, only slight and insignificant decreases in the renal blood flow from 224+/-16 to 203+/-19 ml/min and renal vascular resistance from 0.66+/-0.06 to 0.61+/-0.05 arbitrary resistance units (ru) were observed during inflation of the balloon. Concomitant with these hemodynamic changes, plasma renin activity and plasma norepinephrine concentration increased significantly in both the arterial and renal venous bloods. Plasma concentration of prostaglandin E(2) in renal venous blood increased from 34+/-6 to 129+/-24 pg/ml (P < 0.01). The subsequent administration of indomethacin or meclofenamate had no significant effect on mean arterial pressure, cardiac output, and total peripheral vascular resistance, but reduced renal blood flow from 203+/-19 to 156+/-21 ml/min (P < 0.01) and increased renal vascular resistance from 0.61+/-0.05 to 1.05+/-0.21 ru (P < 0.01). Simultaneously, the plasma concentration of prostaglandin E(2) in renal venous blood fell from 129+/-24 to 19+/-3 pg/ml (P < 0.01). Administration of indomethacin to five dogs without prior obstruction of the inferior vena cava had no effect upon renal blood flow or renal vascular resistance. The results indicate that acute reduction of cardiac output enhances renal renin secretion and the activity of the renal adrenergic nerves as well as renal prostaglandin synthesis without significantly changing renal blood flow or renal vascular resistance. Inhibition of prostaglandin synthesis during acute reduction of cardiac output results in an increased renal vascular resistance and reduced renal blood flow. Accordingly, that data provide evidence that renal prostaglandins counteract in the kidney the vasoconstrictor mechanisms activated during acute reduction of cardiac output.

Renal effects of drugs that inhibit prostaglandin synthesis

There is extensive, clinical use of antiinflammatory drugs that inhibit prostaglandin synthesis in most, if not all, organs in the body. Much of the therapeutic efficacy of these agents depends on a reduction of prostaglandin synthesis at the site of inflammation. Not surprisingly, many of the side-effects of these drugs are secondary to decreased prostaglandin synthesis in brain, vasculature, stomach, lung, and kidney. In this review, we will focus attention on the effects of these antiinflammatory compounds on renal function, with particular emphasis on renin secretion, control of renal blood flow (RBF), and glomerular filtration rate (GFR). To describe these renal consequences of prostaglandin inhibition, we will briefly review the biochemistry of prostaglandin synthesis and the major known physiologic actions of prostaglandins in the kidney.

The actions of dopamine and of sulpiride on regional blood flows in the rat kidney.

1. Blood flow was measured in the renal cortex and medulla of anaesthetized rats by the hydrogen washout method. The effects of dopamine infusion were measured. 2. Low doses of dopamine (20 and 65 n-mole.kg-1.min-1) caused only small increases in renal blood flow, and a higher dose (200 n-mole.kg-1.min-1) caused vasoconstriction. After alpha-blockade with phenoxybenzamine (9 mumole.kg-1), all doses of dopamine caused vasodilatation in the cortex and medulla of the kidney. 3. This dopamine-induced renal vasodilatation was almost abolished by sulpiride (0.7 mumole.kg-1.min-1), but was only slightly attenuated by propranolol (10 mumole.kg-1). 4. Sulpiride did not significantly alter the renal blood flow responses to noradrenaline or isoprenaline, or the blood pressure responses to histamine, acetylcholine, 5HT, noradrenaline and isoprenaline. 5. In normal rats, infusion of sulpiride generally caused a reduction in renal cortical blood flow. This response showed a positive correlation with the initial blood pressure. 6. It is concluded that there are specific dopamine receptors in the renal vasculature of the rat, and that dopamine may play a role in the normal control of renal blood flow.

Parabrachial pons mediates hypothalamically induced renal vasoconstriction.

The role of the parabrachial region of the dorsal rostral pons (PB) in mediating control of renal blood flow and of systemic arterial blood pressure was investigated in nine cats anesthetized with chloralose-urethan. Electrical stimulation through electrodes placed stereotaxically in lateral and medial positions in the hypothalamus (LH and MH) in PB and in ventrolateral reticular formation (VLRF) of each cat elicited pronounced systemic arterial pressor responses and renal vasoconstrictions. Stimulation parameters were adjusted so that renal flow responses elicited from each site were equal. Following a unilateral lesion in the PB, responses of renal vasoconstriction induced by hypothalamic stimulation were attenuated, but responses of arterial pressure were not altered. Stimulation of the VLRF, posterior to the lesion, consistently produced undiminished systemic pressor responses and renal vasoconstriction throughout the durations of the experiments excluding decay of renal vascular responsiveness. Thus, the data suggest that pathways mediating renal vasoconstriction in response to hypothalamic stimulation was discrete and pass through the parabrachial region, whereas pathways mediating systemic vasoconstriction in response to hypothalamic stimulation are distinct or less compact.

A Control system model of renal blood flow regulation

A dynamic mathematical model of renal blood flow control is developed based upon a comprehensive model of the renal medulla. The model reproduces observed dynamic features of response and provides insight into their physiological basis.

The effect of noradrenaline, adrenergic blocking agents, and tyramine on the intrarenal distribution of blood flow in the baboon

The intrarenal distribution of blood flow in the baboon was measured using the 133xenon clearance technique, and dose-response curves for the various components of renal blood flow were determined during intra-arterial infusions of noradrenaline; the alpha-adrenergic blocking agent, phenoxybenzamine; the beta-adrenergic blocking agent, propranolol; and tyramine which causes the release of endogenous NA. High doses of noradrenaline reduced flow in the outer cortex; this effect was attenuated by phenoxybenzamine, but not by propranolol. Tyramine had no effect. These r results suggest that there are alpha-adrenergic receptors in the resistance vessels of the kidney but are inconsistent with an important role for NA-mediated autonomic control of renal blood flow.

Renal Physiology.

This book on renal physiology does what it purports to do. It has been developed as an introductory guide for first year medical students and advanced undergraduate students. It is a well-organized, succinct presentation of renal physiology. The book will also serve practicing physicians who find it difficult to retain information concerning pH and salt and water balance, and who may not have been exposed to recent information about countercurrent mechanisms, micropuncture technique, and control of the renal circulation. The author handles controversial areas deftly by emphasizing what is established fact and by stating with equal clarity and brevity those issues that are still in doubt. Another positive aspect is the author's success in not repeating once-told information. Each of the 12 chapters is preceded by a synopsis. Renal structure, historical review, body fluids and electrolyte composition, glomerular filtration, renal blood flow, control of renal blood flow and glomerular filtration

Sympathetic nerve activity to the spleen, kidney, and heart in response to baroceptor input.

Sympathetic nerve activity to the spleen, kidney, and heart in response to baroceptor input.

A PROGRESS REPORT OF INVESTIGATIONS CONCERNED WITH THE EXPERIMENTAL TREATMENT OF HYPERTENSION WITH KIDNEY EXTRACTS

Excerpt At this time last year we reported to you the reasons why we believe that certain extracts of normal kidneys contain a substance, or substances, which lowers arterial blood pressure in hype...