The effects of combined renal vasodilatation and pressor agents on renal hemodynamics and the tubular reabsorption of sodium.

Earley, Laurence E.; Friedler, Robert M.

doi:10.1172/jci105368

Cited by 214 publications

(111 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Low doses of dopamine cause diuresis and 449 IS PHY 292 450 B. J. CHAPMAN AND OTHERS natriuresis in all three species. In the present study it was observed that a subpressor dose of dopamine had a greater vasodilator action on renal medullary blood flow than on cortical blood flow, and this action on the renal medulla may contribute to the diuretic and natriuretic actions of dopamine (see Earley & Friedler, 1966). There is also other evidence suggesting that dopamine causes natriuresis by its action on the renal blood vessels, since May & Carter (1970) have suggested that dopamine has little or no action on tubular function because it was ineffective when injected into the portal vessels of the chicken.…”

Section: Discussionmentioning

confidence: 61%

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

Chapman¹,

Horn²,

Munday³

et al. 1980

The Journal of Physiology

View full text Add to dashboard Cite

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.

show abstract

Section: Discussionmentioning

confidence: 61%

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

Chapman¹,

Horn²,

Munday³

et al. 1980

The Journal of Physiology

View full text Add to dashboard Cite

show abstract

“…In the absence of medullary autoregulation pressure will rise in those capillaries which originate from the juxtamedullary glomeruli and surround the short loops of Henle. As proposed by Earley et al (34,35) and Lewy and Windhager (36), such a change in the hydrostatic pressure gradient could result in a reduction of sodium and water reabsorption. Furthermore, as already mentioned, juxtamedullary filtration rate is strikingly elevated in chronic hypertension (30).…”

Section: Methodsmentioning

confidence: 89%

Fluid reabsorption in Henle's loop and urinary excretion of sodium and water in normal rats and rats with chronic hypertension

Stumpe¹,

Lowitz²,

Ochwadt³

1970

J. Clin. Invest.

View full text Add to dashboard Cite

A B S T R A C T The function of the short loops of Henle was investigated by micropuncture technique in normal rats, in rats with spontaneous hypertension, and in the untouched kidney of rats with experimental renal hypertension. All animals received a standard infusion of 1.2 ml of isotonic saline per hr.With increasing arterial blood pressure (range from 90 to 220 mm Hg), a continuous decrease in transit time of Lissamine green through Henle's loop from 32 to 10 sec was observed. Fractional water reabsorption along the loop declined progressively from 26 to 10%, and fractional sodium reabsorption decreased from 40 to 36% of the filtered load. The fluid volume in Henle's loop calculated from transit time and mean flow rate also decreased with increasing blood pressure. There was no change in superficial single nephron filtration rate but there was a slight increase in total glomerular filtration rate (GFR). Sodium and water reabsorption in the proximal tubule remained unchanged.Urine flow rate, sodium excretion, osmolar clearance, and negative free water clearance increased with increasing blood pressure. The osmolal urine to plasma (U/P) ratio declined but did not fall below a value of 1.5. It is concluded that the increase in sodium and water excretion with chronic elevation of arterial blood pressure is caused by a decrease of sodium and water reabsorption along the loop of Henle, presumably as a consequence of increased medullary blood pressure. The following three groups of animals were used: (a) normal rats, (b) rats with a moderate spontaneous hypertension, and (c) rats with experimental hypertension 4-5 wk after clamping one renal artery with a Goldblatt clamp. In the last group, only the untouched kidney, which is exposed to the high blood pressure, was investigated. All animals received an isotonic saline infusion of 1.2 ml/hr. Micropuncture experiments were done on superficial nephrons. Accordingly, only the function of short loops of Henle was studied. METHODSThe experiments were performed on Albino rats of about the same weight (190-210 g). The animals were divided into three groups differing from each other by the level of arterial blood pressure. For the first group male rats-of the FW4, strain (Paderborn) were chosen, having a mean arterial blood pressure between 90 and 110 mm Hg. The second group consisted of female rats of the Wistar strain with a blood pressure from 110 to 160 mm Hg. In the third group female Wistar rats with experimental renal hypertension of 4-5 wk duration (for the method see reference 12, 13) were used, their blood pressure ranging from 160 to 220 mm Hg. In this last group only the untouched kidney exposed to the high arterial blood pressure was investigated. All animals were kept on the same standard rat diet (Altromin, sodium content: 1200 mg/kg) and had free access to water. The animals were anaesthetized by intraperitoneal injection of Inactin Hamburg,(70)(71)(72)(73)(74)(75)(76)(77)(78)(79)(80) mg/kg body weight) and prepared for micropuncture as previously describe...

show abstract

“…With regard to this latter change, they suggested that the distensibility of the proximal tubule might be limited during rapid saline infusion because of an increase in hydrostatic pressure, or a fall in colloid oncotic pressure in the peritubular capillaries, and a resultant increase in interstitial volume proximal tubular volume to GFR/nephron. (26,28,29). The rise in GFR which often occurs in the rat during saline loading would thus not be accompanied by a proportionate increase in the volume of the proximal tubule.…”

Section: Discussionmentioning

confidence: 99%

Effect of changes in renal perfusion pressure on the suppression of proximal tubular sodium reabsorption due to saline loading

Bank¹,

Koch²,

Aynedjian³

et al. 1969

J. Clin. Invest.

View full text Add to dashboard Cite

AIB S T R A C T Rapid intravenous infusion of saline isknown to suppress reabsorption of sodium and water in the proximal tubule. It has previously been shown that this suppression is accompanied by two changes which in combination might account for the over-all decrease in reabsorption: a reduction in the intrinsic reabsorptive capacity of the tubular epithelium (C/rr') and a reduction in the ratio between tubular volume and GFR (7rrd/Vo). The present micropuncture experiments were carried out in order to study the possible role of altered peritubular physical forces (hydrostatic and colloid oncotic pressure) in mediating these two changes. Proximal tubular reabsorptive capacity, transit time, fractional reabsorption of sodium and water, 7rrd/Vo, and intratubular hydrostatic pressure were measured in salineloaded rats during acute changes in renal perfusion pressure induced by intermittent constriction of the abdominal aorta.We found that when renal perfusion pressure was lowered to 70-90 mm Hg, the usual effects of saline loading on C/irr, 7rrd/Vo, and fractional reabsorption in the proximal tubule were greatly minimized. When the aortic clamp was released and renal perfusion pressure allowed to rise, C/irr', 7rrd/Vo, and fractional reabsorption fell markedly to levels characteristically seen in saline diuresis. Reclamping of the aorta reversed all of these changes.In order to determine whether the changes in C/rr' accompanying changes in renal perfusion pressure were mediated by a circulating natriuretic hormone, we assayed in hydopenic rats the dialysate of plasma collected from saline-loaded rats during and after release of aortic constriction by the split oil drop method. No Dr. Norman Bank is a Career Scientist of the Health Research Council of New York City.Received for publication 21 June 1968 and in revised form 9 October 1968. significant difference in reabsorptive half-time (ti) was found between the two dialysates, and ti with both dialysates was approximately the same as was found when isotonic saline was injected in the tubules of hydropenic control animals. These observations suggest that the large changes in C/rr' which occurred with changes in renal perfusion pressure in saline-loaded rats were not mediated by a circulating hormone. We suggest that the reduction in C/ir', wr'd/Vo, and fractional reabsorption which occurs in the proximal tubule during a saline diuresis is related to the rise in hydrostatic pressure within the kidney. INTRODUCTIONIt is now well established that the increase in urinary excretion of sodium which occurs during acute saline loading is due to a decrease in sodium reabsorption by the tubules rather than to an increase in the amount of sodium filtered by the glomeruli (1-8). The mechanism (or mechanisms) responsible for this decrease in tubular reabsorption is not entirely clear. It has been shown by Rector, Sellman, Martinez-Maldonado, and Seldin (9) that acute saline loading in the rat is accompanied by two changes in the proximal tubule: a reduction in the intrins...

show abstract

The effects of combined renal vasodilatation and pressor agents on renal hemodynamics and the tubular reabsorption of sodium.

Cited by 214 publications

References 18 publications

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

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

Fluid reabsorption in Henle's loop and urinary excretion of sodium and water in normal rats and rats with chronic hypertension

Effect of changes in renal perfusion pressure on the suppression of proximal tubular sodium reabsorption due to saline loading

Contact Info

Product

Resources

About