The Release of Renin into the Renal Circulation of the Anaesthetized Dog

1970 ◽  
Vol 38 (2) ◽  
pp. 157-174 ◽  
Author(s):  
K. F. Hosie ◽  
J. J. Brown ◽  
A. M. Harper ◽  
A. F. Lever ◽  
R. F. MacAdam ◽  
...  
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Plasma Renin ◽  
Renin Release ◽  
Concentration Difference ◽  
Plasma Renin Concentration ◽  
Renal Lymph ◽  
Arterial Blood ◽  
Arterial Plasma ◽  
Venous Plasma

1. In anaesthetized dogs the rate at which renin was released into the circulation of the right and left kidneys was estimated from renal blood flow, haematocrit, and the V-A renin concentration difference across the kidney. Renin was also measured in samples of renal lymph collected at the same time. 2. The effect on renin release of reducing blood flow in one kidney was studied. For all observations (control and experimental), renal venous plasma renin concentration (RVR) was directly related to arterial plasma renin concentration and to renin release; RVR was inversely related to renal plasma flow. 3. The concentration of renin in renal lymph was considerably higher than that in renal venous plasma taken at the same time. Arterial plasma renin concentration was directly related to the sum of the rates at which renin was released from the two kidneys. 4. Clamping the renal artery of one kidney for 1 hr led to a marked reduction of renal blood flow, to a marked increase in RVR and to a variable change in renin release. Removal of the clamp was followed by increased renin release and by reversal of a previously positive V-A renin difference in the control kidney. 5. On several other occasions negative V-A renin differences were observed. That is, more renin appeared to enter the kidney in arterial blood than left in the renal vein.

Plasma ATP during exercise: possible role in regulation of coronary blood flow

2005 ◽  
Vol 288 (4) ◽  
pp. H1586-H1590 ◽  
Author(s):  
Martin Farias ◽  
Mark W. Gorman ◽  
Margaret V. Savage ◽  
Eric O. Feigl
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Oxygen Tension ◽  
Luciferase Assay ◽  
Concentration Difference ◽  
Flow Transducer ◽  
Atp Concentration ◽  
Arterial Plasma ◽  
Myocardial Oxygen Extraction ◽  
Venous Plasma

It was previously shown that red blood cells release ATP when blood oxygen tension decreases. ATP acts on microvascular endothelial cells to produce a retrograde conducted vasodilation (presumably via gap junctions) to the upstream arteriole. These observations form the basis for an ATP hypothesis of local metabolic control of coronary blood flow due to vasodilation in microvascular units where myocardial oxygen extraction is high. Dogs ( n = 10) were instrumented with catheters in the aorta and coronary sinus, and a flow transducer was placed around the circumflex coronary artery. Arterial and coronary venous plasma ATP concentrations were measured at rest and during three levels of treadmill exercise by using a luciferin-luciferase assay. During exercise, myocardial oxygen consumption increased ∼3.2-fold, coronary blood flow increased ∼2.7-fold, and coronary venous oxygen tension decreased from 19 to 12.9 mmHg. Coronary venous plasma ATP concentration increased significantly from 31.1 to 51.2 nM ( P < 0.01) during exercise. Coronary blood flow increased linearly with coronary venous ATP concentration ( P < 0.01). Coronary venous-arterial plasma ATP concentration difference increased significantly during exercise ( P < 0.05). The data support the hypothesis that ATP is one of the factors controlling coronary blood flow during exercise.

Effect of intrarenal administration of dopamine on renin release in conscious dogs

1983 ◽  
Vol 244 (1) ◽  
pp. H39-H45 ◽  
Author(s):  
H. Mizoguchi ◽  
V. J. Dzau ◽  
L. G. Siwek ◽  
A. C. Barger
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Adrenergic Receptors ◽  
Dose Range ◽  
Plasma Renin ◽  
Systemic Blood Pressure ◽  
Conscious Dogs ◽  
Renin Release ◽  
Dopamine Antagonists ◽  
Vasodilatory Action

We investigated the effect of intrarenal administration of dopamine on renin release in conscious dogs. Dopamine in doses ranging from 0.28 to 3.0 micrograms . kg(-1) . min(-1) produced a significant increase in systemic plasma renin activity (PRA) and renin secretion rate without altering systemic blood pressure. Dopamine also induced renal vasodilatation and natriuresis within this dose range. To determine if the dopamine-induced renin release is related to its vasodilatory action, two other vasodilators, papaverine and acetylcholine, were infused into the renal artery, but neither, in doses that produced a rise in renal blood flow similar to that of dopamine, had any effect on PRA. As dopamine can activate alpha- and beta-adrenergic receptors in addition to dopaminergic receptors, experiments were also performed to characterize the type of receptors involved in dopamine-induced renin release. Intrarenal infusion of sulpiride and haloperidol, dopamine antagonists, significantly inhibited dopamine-induced renin release and renal vasodilatation. In contrast, intrarenal infusion of propranolol failed to alter dopamine-induced rise in PRA or renal blood flow. Simultaneous infusion of phentolamine and dopamine, on the other hand, produced a significant potentiation of dopamine-induced renin release and renal vasodilatation. In conclusion, our studies demonstrate that dopamine is capable of inducing renin release and renal vasodilatation in conscious dogs. Moreover, such actions of dopamine are mediated through activation of specific dopamine receptors in the kidney. Finally, we present evidence for the existence of the intrarenal alpha-adrenergic mechanism that is inhibitory to renin release.

Long-Term versus Short-Term Effects of Hydrochlorothiazide on Renal Haemodynamics in Essential Hypertension

1979 ◽  
Vol 56 (5) ◽  
pp. 463-469 ◽  
Author(s):  
P. Van Brummelen ◽  
M. Woerlee ◽  
M. A. D. H. Schalekamp
Keyword(s):  
Blood Flow ◽  
Essential Hypertension ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Plasma Renin ◽  
Renal Vascular Resistance ◽  
Vanillylmandelic Acid ◽  
Plasma Renin Concentration ◽  
Renal Vascular

1. Renal blood flow, glomerular filtration rate, renal vascular resistance and filtration fraction were studied in ten patients with essential hypertension, during placebo, and after 1 week, 3, 6 and 9 months of hydrochlorothiazide. Plasma renin concentration and urinary excretion of vanillylmandelic acid were also measured. 2. Mean arterial pressure was lowered significantly during hydrochlorothiazide, the long-term effect being slightly more pronounced than the short-term effect. 3. The decrease in renal blood flow during the first week (P < 0·01) was followed by a progressive rise. After 9 months renal blood flow was above placebo level in eight of the ten patients. After an initial decrease, glomerular filtration rate returned gradually to its original value. Renal vascular resistance and filtration fraction increased during the first week and declined thereafter. After 3, 6 and 9 months renal vascular resistance was significantly lower compared with placebo values. 4. Plasma renin concentration and urinary excretion of vanillylmandelic acid increased significantly during the first week of hydrochlorothiazide. Subsequently, vanillylmandelic acid fell to below pretreatment amounts (P < 0·05), whereas plasma renin concentration remained elevated. 5. Long-term treatment of essential hypertension with hydrochlorothiazide has a favourable effect on abnormal renal haemodynamics. Besides the influence of blood pressure reduction per se, humoral and neural factors may be involved.

Dependence of Renal Vasodilator Effect of Captopril on Prevailing Plasma Renin Level in the Dog: Influence of DOCA–Salt Treatment

1982 ◽  
Vol 63 (4) ◽  
pp. 355-360 ◽  
Author(s):  
P. C. Wong ◽  
B. G. Zimmerman
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Plasma Renin Activity ◽  
Renal Blood Flow ◽  
Plasma Renin ◽  
High Salt ◽  
Renin Activity ◽  
Arterial Blood ◽  
Low Salt ◽  
Renin Level

1. The blood pressure and renal blood flow response to captopril (0·2 mg/kg, intravenously) was studied in low salt, normal, and high salt fed conscious dogs, and in a group of DOCA-salt treated dogs. 2. Mean arterial blood pressure was decreased and renal blood flow increased most in the low salt group, but significant changes were also obtained in the normal group. The high salt and DOCA-salt groups were only marginally affected by captopril. 3. When the data from all four groups of dogs were subjected to regression analysis, there was a significant relationship (r = 0·68) between the prevailing plasma renin activity and the increase in renal blood flow caused by captopril. 4. The results suggest that renal vasodilatation resulting from converting enzyme inhibition is mainly due to a decrease in the level of circulating angiotensin II, and that even in the normal conscious dog the prevailing plasma renin activity can affect blood pressure and renal blood flow.

Renal actions of neuropeptide Y in the primate

1989 ◽  
Vol 256 (4) ◽  
pp. F524-F531 ◽  
Author(s):  
S. F. Echtenkamp ◽  
P. F. Dandridge
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Neuropeptide Y ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Plasma Renin ◽  
Arterial Plasma ◽  
Dose Dependent

Neuropeptide Y (NPY) is a potent vasoconstrictor peptide contained in sympathetic nerve terminals and is co-released with norepinephrine. Previous studies in the rat have suggested that NPY influences renal sodium reabsorption and renin release. However, little is known about the physiological effects of NPY on the kidney in the human. In the present study NPY was infused intravenously and directly into the renal artery of the primate Macaca fascicularis, an experimental model of the human. Intravenous NPY infusion at doses of 20-1,000 ng.kg-1.min-1 produced dose-dependent rises in renal vascular resistance with minimal changes in arterial pressure. Urine flow and sodium excretion were changed significantly only at doses of NPY that significantly reduced renal blood flow and filtration rate. Arterial plasma renin activity and renin secretion rate were not significantly altered at any dose of NPY. Intrarenal infusion of NPY at doses of 20-400 ng.kg-1.min-1 produced potent dose-dependent renal vasoconstriction with minimal changes in arterial pressure. Under these conditions sodium excretion was significantly reduced concurrent with decreases in renal blood flow and glomerular filtration rate. However, no significant changes in arterial plasma renin activity or renin secretion rate were found at any dose of NPY. These data indicate that in the nonhuman primate NPY is a potent renal vasoconstrictor agent that has variable effects on renal excretory and secretory function, which may be secondary to its vasoconstrictor actions.

Effect of KCl infusion on renin secretory rates and aldosterone excretion in dogs

1975 ◽  
Vol 229 (2) ◽  
pp. 370-375 ◽  
Author(s):  
W Flamenbaum ◽  
JG Kleinman ◽  
JS McNeil ◽  
RJ Hamburger ◽  
TA Kotchen
Keyword(s):  
Blood Flow ◽  
Plasma Renin Activity ◽  
Renal Blood Flow ◽  
Flow Distribution ◽  
Plasma Renin ◽  
Systemic Blood Pressure ◽  
Renin Activity ◽  
Secretory Rate ◽  
Arterial Plasma ◽  
Renal Blood Flow Distribution

The effects of unilateral intrarenal arterial KCl infusion in dogs (12 mueq/kg per min) on bilateral renal function, renin secretory rates, and aldosterone excretion were studied. During KCl infusion, infused-side renal arterial plasma [K+] increased by 2.2 +/- 0.6 meq/liter. Systemic plasma [K+] simultaneously rose by 0.6 +/- 0.1 meq/liter. Plasma renin activity decreased 29 +/- 9%, and the decrease correlated with the increases in plasma [K+]. Renin secretory rate decreased bilaterally, the decrease being greater in each experiment on the infused side. Aldosterone excretion increased during KCl infusion by 72 +/- 17%, despite a decrease in plasma renin activity. With KCl infusion there was a bilateral increase in K+ excretion, and a positive correlation was observed between the net alterations in K+ and Na+ excretion. No significant alterations in systemic blood pressure, glomerular filtration rate, total renal blood flow, or intracortical renal blood flow distribution were observed. These studies suggest that K+ inhibits the release of renin by an intrarenal mechanism, which may be related to a K+-induced alteration in Na+ absorption.

Haemodynamic Characteristics of Low-Renin Hypertension

1977 ◽  
Vol 52 (4) ◽  
pp. 405-412 ◽  
Author(s):  
M. A. D. H. Schalekamp ◽  
W. H. Birkenhäger ◽  
G. A. Zaal ◽  
G. Kolsters
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Plasma Renin ◽  
Renal Vascular Resistance ◽  
Plasma Renin Concentration ◽  
Low Renin Hypertension ◽  
Renal Vascular ◽  
The Relationship

1. Intra-arterial pressure, cardiac output, renal blood flow and glomerular filtration rate were measured in 19 patients with low-renin hypertension and in 30 patients with normal-renin hypertension. 2. Cardiac output and renal blood flow were significantly lower in low-renin hypertension. Total peripheral and renal vascular resistance were markedly higher in this group. 3. Plasma renin concentration correlated inversely with both total peripheral and renal vascular resistance as well as with age. Multiple regression analysis indicated that part of the relationship between renin and haemodynamic variables did not depend on age. Furthermore, plasma renin concentration did not decrease with age in a group of 40 normotensive control subjects of similar age to the hypertensive patients. 4. The results provide further confirmation that renin decreases as hypertension progresses.

Renal responses to mental stress and epinephrine in humans

1989 ◽  
Vol 257 (4) ◽  
pp. F682-F689 ◽  
Author(s):  
B. Tidgren ◽  
P. Hjemdahl
Keyword(s):  
Blood Flow ◽  
Sympathetic Nerve ◽  
Mental Stress ◽  
Sympathetic Nerve Activity ◽  
Renin Release ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Arterial Plasma ◽  
Renal Sympathetic ◽  
Venous Plasma

Renal blood flow, renal sympathetic nerve activity, and renin release responses to mental stress (Stroop's color-word conflict test; CWT) and intravenously infused epinephrine (Epi) were evaluated in 12 healthy volunteers. The overflows of norepinephrine (NE) and dopamine (DA) to renal venous plasma were measured as indexes of nerve activity; the fractional extraction of Epi was used to assess renal catecholamine extraction from arterial plasma. At rest, NE and DA levels were higher in renal venous plasma than in arterial plasma. Arterial Epi levels were 0.26 +/- 0.04 nmol/l, and the fractional extraction of Epi by the kidney was 46 +/- 4%. CWT increased renal vascular resistance (RVR) by 48%, renal venous NE overflow by 214% (to 708 +/- 79 pmol/min), and DA overflow by 42% (to 34 +/- 4 pmol/min). Arterial Epi increased by 197%. The vasoconstrictor response was correlated with the NE overflow response. The increased renin release (from 75 to 247 U/min, median values; P less than 0.001) was correlated to increases in mean arterial pressure and NE and DA overflows. Epi infusion increased arterial plasma Epi and renin release dose dependently to 6.43 +/- 0.27 nmol/l and by 664%, respectively. RVR and NE and DA overflows were unchanged. Renal venous DA data support the existence of a subset of renal dopaminergic nerves. Mental stress causes renal vasoconstriction, apparently due to increased renal sympathetic nerve activity. Physiological increments of circulating Epi do not affect renal blood flow but enhance renin release markedly without apparent activation of the renal nerves in humans.

Renal blood flow changes in contralateral kidney of Goldblatt hypertensive dog

1981 ◽  
Vol 241 (2) ◽  
pp. H145-H148
Author(s):  
B. G. Zimmerman ◽  
C. Mommsen
Keyword(s):  
Blood Flow ◽  
Renal Artery ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Control Level ◽  
Plasma Renin ◽  
Renal Vascular Resistance ◽  
Contralateral Kidney ◽  
Arterial Blood ◽  
Renal Vascular

Sequential changes in systemic arterial blood pressure (BP), renal blood flow (RBF) in the contralateral kidney, and plasma renin activity (PRA) were examined on conscious dogs with construction of a single renal artery (RAC). An increase of 24 mmHg in bP occurred within 2 days after RAC, and BP later plateaued at a lower level. RBF in the contralateral kidney transiently increased by 24% and then returned to the control level in 11-14 days. PRA also peaked early after RAC and then returned to control. The clamp was tightened and the renal artery was occluded (RAO) 3-20 days after RAC. BP, RBF, and PRA increased to an even greater degree than after RAC. BP peaked at 145 mmHg, and RBF increased 61.5% at 2-3 days after RAO. BP and RBF both decreased but remained above the control for the duration of the study, BP at 127 mmHg and RBF at 256 ml/min. RBF per gram for the hypertrophied contralateral kidney was calculated from the RBF before death and the weight at death. The final RBF per gram of the contralateral kidney (2.7 ml.min-1.g-1) decreased and renal vascular resistance increased compared with the estimated control RBF/g (3.7 ml.min-1.g-1) and renal vascular resistance. These results suggest that the final RBF of the contralateral kidney is not increased in proportion to its increase in weight and that it may be relatively hypoperfused in two-kidney one-clip Goldblatt hypertension.

Vasodilator capacity of contralateral kidney in Goldblatt hypertensive dog

1983 ◽  
Vol 245 (5) ◽  
pp. H790-H795
Author(s):  
B. G. Zimmerman ◽  
R. D. Largent
Keyword(s):  
Blood Flow ◽  
Renal Artery ◽  
Renal Blood Flow ◽  
Control Level ◽  
Plasma Renin ◽  
Artery Occlusion ◽  
Angiotensin I ◽  
Contralateral Kidney ◽  
Arterial Blood ◽  
Renal Artery Occlusion

Because of previous suggestions of impaired renal blood flow in the contralateral kidney of Goldblatt hypertensive animals, we examined the maximal vasodilator capacity of the contralateral kidney in 13 instrumented dogs during progression of Goldblatt hypertension. Constriction of a single renal artery (RAC) followed a week or more later by total renal artery occlusion (RAO) increased mean arterial blood pressure (BP) from a control level of 102 +/- 3 to 135 +/- 7 mmHg (P less than 0.001) and increased plasma renin activity (PRA) from 0.69 +/- 0.16 to 10.2 +/- 3.9 ng angiotensin I X ml-1 X h-1 (P less than 0.05) at 2 wk after RAO. The hypertension was accompanied by an increase in basal renal blood flow (RBF) from 224 +/- 21 to 300 +/- 27 ml/min (P less than 0.01) and RBF at maximal vasodilatation from 505 +/- 24 to 673 +/- 52 ml/min (P less than 0.05). Hypertension and the increase in PRA waned, but BP remained higher than control at 4 wk after RAO (117 +/- 6 mmHg, P less than 0.005). Basal and maximal RBF were sustained at the higher levels throughout the 4-wk period after RAO. When RBF was expressed on a per gram basis, basal and maximal flow before (3.72 +/- 0.40 and 8.26 +/- 0.62 ml X min-1 X g-1, respectively) did not differ from that in the final experiment after RAO (3.85 +/- 0.34 and 8.19 +/- 0.78 ml X min-1 X g-1). The basal and minimal vascular resistances based on flow per gram were increased by 24 +/- 8 and 41 +/- 16% (P less than 0.05), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

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