Atrial and arterial baroreceptor influences on the circulatory response to acute changes in renal perfusion

1993 ◽  
Vol 71 (7) ◽  
pp. 425-431
Author(s):  
N. Ashton ◽  
A. J. Rankin
Keyword(s):  
Vascular Resistance ◽  
Left Atrial ◽  
Perfusion Pressure ◽  
Carotid Sinus ◽  
Renal Perfusion ◽  
Receptor Stimulation ◽  
Renal Perfusion Pressure ◽  
Atrial Receptor ◽  
Acute Changes ◽  
Atrial Receptors

We have recently reported a neurally mediated reflex increase in hindlimb vascular resistance associated with an acute decrease in renal perfusion pressure in the chloralose–urethane-anesthetized rabbit. The present study was designed to investigate the influence of this reflex in the body's integrated response to circulatory disturbances by investigating the influence of carotid baroreceptor and left atrial receptors on this reflex and assessing the effect of acute changes in renal perfusion on the heart. Interaction of the renal-generated reflex with carotid baroreceptors was investigated by independent perfusion of the carotid sinus region. Responses in hindlimb perfusion pressure, at constant flow, to changes in renal perfusion were greatest with the carotid sinus perfusion pressure (CSP) low (27 ± 4 mmHg (1 mmHg = 133.3 Pa) increase in hindlimb pressure at low CSP vs. 19 ± 3 mmHg increase at normal CSP) and were inhibited with maximum carotid stimulation. Partial mitral obstruction, resulting in left atrial distension and atrial receptor stimulation, attenuated the hindlimb vascular response. The increase in hindlimb pressure under control conditions was 34 ± 10 mmHg compared with 20 ± 5 mmHg during atrial receptor stimulation. However, acute reduction of renal perfusion pressure did not result in any changes in heart rate, cardiac output, or inotropic state. It appears that both atrial and arterial baroreflexes modify the reflex change in hindlimb vascular resistance associated with acute alterations of renal perfusion.Key words: afferent renal nerves, baroreceptors, atrial receptors, vascular resistance.

Effect of renal perfusion pressure on sodium reabsorption from proximal tubules of superficial and deep nephrons

1986 ◽  
Vol 250 (3) ◽  
pp. F425-F429 ◽  
Author(s):  
J. A. Haas ◽  
J. P. Granger ◽  
F. G. Knox
Keyword(s):  
Proximal Tubule ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Proximal Tubules ◽  
Sodium Reabsorption ◽  
Renal Perfusion Pressure ◽  
Henle's Loop ◽  
Acute Change ◽  
Acute Changes ◽  
Superficial And Deep Nephrons

Previous studies in rats have demonstrated that superficial proximal tubule sodium reabsorption does not change in response to alterations in renal perfusion pressure (RPP). The first objective of the present study was to estimate sodium reabsorption in response to acute changes in RPP utilizing fractional lithium reabsorption (FRLi) as an index of fractional sodium reabsorption (FRNa) by the proximal tubule of the kidney as a whole. FRLi decreased in response to increases in RPP, suggesting that sodium reabsorption by the proximal tubule of some nephron population is decreased. Therefore, the second objective of the present study was to test the hypothesis that superficial and deep proximal tubules respond differently to changes in RPP by comparing proximal tubule sodium reabsorption from both nephron populations. In response to an acute change in RPP from 114 +/- 4 to 138 +/- 5 mmHg, FRNa by the proximal tubule and descending limb of Henle's loop in deep nephrons decreased from 71.3 +/- 2.3 to 55.8 +/- 5.6%, but FRNa by the superficial late proximal tubule was not changed: (44.3 +/- 4.8 to 45.1 +/- 3.9%). The urinary fractional reabsorption of sodium decreased from 96.7 +/- 0.6 to 94.5 +/- 0.5%. In summary, these studies demonstrate that increases in RPP have no effect on sodium reabsorption by the proximal tubule of superficial nephrons. In contrast, sodium delivery to the point of micropuncture in the descending limb of Henle's loop of deep nephrons was increased, suggesting inhibition of sodium reabsorption by proximal tubules of deep nephrons in response to increases in RPP.

Effects of renal perfusion pressure on the natriuresis induced by atrial natriuretic factor

1987 ◽  
Vol 253 (2) ◽  
pp. F234-F238
Author(s):  
A. A. Seymour ◽  
S. G. Smith ◽  
E. K. Mazack
Keyword(s):  
Vascular Resistance ◽  
Atrial Natriuretic Factor ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renal Vascular Resistance ◽  
Base Line ◽  
Renal Perfusion Pressure ◽  
Natriuretic Factor ◽  
Renal Vascular ◽  
Atrial Natriuretic

Synthetic atrial natriuretic factor (ANF 101-126) was infused at 1, 5, 25, and 125 pmol X kg-1 X min-1 into the renal artery of anesthetized, one-kidney dogs. During administration of 25 and 125 pmol X kg-1 X min-1 of ANF 101-126, fractional sodium excretion (FENa) rose from 1.4 +/- 0.3 to 6.6 +/- 1.1 and 5.6 +/- 1.3% when renal perfusion pressure (RPP) was at its basal level (112 +/- 5 mmHg). When base-line RPP was lowered to 101 +/- 5 mmHg by tightening a suprarenal aortic constriction, the same doses raised FENa to only 5.6 +/- 1.6 and 5.1 +/- 1.6%. A larger reduction of beginning RPP to 82 +/- 4 mmHg suppressed the natriuretic responses to 25 and 125 pmol X kg-1 X min-1 of ANF 101-126 to only 1.4 +/- 0.8 and 0.8 +/- 0.3%, respectively.During the peak natriuretic dose of 25 pmol X kg-1 X min-1, renal vascular resistance (RVR) fell from 0.88 +/- 0.10 to 0.68 +/- 0.07, from 0.78 +/- 0.10 to 0.68 +/- 0.12, and from 0.60 +/- 0.06 to 0.61 +/- 0.06 mmHg X ml-1 X min-1 at RPP = RPP = 112, 101, and 82 mmHg, respectively. ANF 101-126 did not affect glomerular filtration rate (GFR) at any level of RPP tested. In conclusion, the natriuretic responses to ANF 101-126 occurred without changes in GFR and were modulated by the prevailing levels of renal perfusion pressure and renal vascular resistance.

Interaction of renal beta 1-adrenoceptors and prostaglandins in reflex renin release

1983 ◽  
Vol 244 (4) ◽  
pp. F418-F424 ◽  
Author(s):  
U. Kopp ◽  
G. F. DiBona
Keyword(s):  
Sodium Excretion ◽  
Perfusion Pressure ◽  
Carotid Sinus ◽  
Urinary Sodium Excretion ◽  
Renal Perfusion ◽  
Prostaglandin Synthesis ◽  
Urinary Sodium ◽  
Secretion Rate ◽  
Renin Secretion ◽  
Renal Perfusion Pressure

Anesthetized dogs with isolated carotid sinus preparation were used to examine the mechanisms involved in the increase in renin secretion rate produced by carotid baroreceptor reflex renal nerve stimulation (RNS) at constant renal perfusion pressure. Lowering carotid sinus pressure by 41 +/- 5 mmHg for 10 min increased mean arterial pressure and heart rate, caused no or minimal renal hemodynamic changes, decreased urinary sodium excretion, and increased renin secretion rate. Metoprolol, a beta 1-adrenoceptor antagonist, given in the renal artery, did not affect the decrease in urinary sodium excretion but attenuated the increase in renin secretion rate, from 1,764 +/- 525 to 412 +/- 126 ng/min (70 +/- 8%). Indomethacin or meclofenamate, prostaglandin synthesis inhibitors, did not affect the decrease in urinary sodium excretion but attenuated the increase in renin secretion rate, from 1,523 +/- 416 to 866 +/- 413 ng/min (51 +/- 18%). Addition of metoprolol to indomethacin-pretreated dogs attenuated the increase in renin secretion rate from 833 +/- 327 to 94 +/- 60 ng/min (86 +/- 10%). These results indicate that reflex RNS at constant renal perfusion pressure results in an increase in renin secretion rate that is largely mediated by renal beta 1-adrenoceptors and is partly dependent on intact renal prostaglandin synthesis. The beta 1-adrenoceptor-mediated increase in renin secretion rate is independent of and not in series with renal prostaglandins.

Role of connexin40 in the autoregulatory response of the afferent arteriole

2012 ◽  
Vol 303 (6) ◽  
pp. F855-F863 ◽  
Author(s):  
Charlotte Mehlin Sorensen ◽  
Isaiah Giese ◽  
Thomas Hartig Braunstein ◽  
Jens Christian Brasen ◽  
Max Salomonsson ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Significant Role ◽  
Knockout Mice ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Tubuloglomerular Feedback ◽  
Wild Type ◽  
Renal Perfusion Pressure ◽  
Acute Changes ◽  
Arteriolar Diameter

Connexins in renal arterioles affect autoregulation of arteriolar tonus and renal blood flow and are believed to be involved in the transmission of the tubuloglomerular feedback (TGF) response across the cells of the juxtaglomerular apparatus. Connexin40 (Cx40) also plays a significant role in the regulation of renin secretion. We investigated the effect of deleting the Cx40 gene on autoregulation of afferent arteriolar diameter in response to acute changes in renal perfusion pressure. The experiments were performed using the isolated blood perfused juxtamedullary nephron preparation in kidneys obtained from wild-type or Cx40 knockout mice. Renal perfusion pressure was increased in steps from 75 to 155 mmHg, and the response in afferent arteriolar diameter was measured. Hereafter, a papillectomy was performed to inhibit TGF, and the pressure steps were repeated. Conduction of intercellular Ca2+changes in response to local electrical stimulation was examined in isolated interlobular arteries and afferent arterioles from wild-type or Cx40 knockout mice. Cx40 knockout mice had an impaired autoregulatory response to acute changes in renal perfusion pressure compared with wild-type mice. Inhibition of TGF by papillectomy significantly reduced autoregulation of afferent arteriolar diameter in wild-type mice. In Cx40 knockout mice, papillectomy did not affect the autoregulatory response, indicating that these mice have no functional TGF. Also, Cx40 knockout mice showed no conduction of intercellular Ca2+changes in response to local electrical stimulation of interlobular arteries, whereas the Ca2+response to norepinephrine was unaffected. These results suggest that Cx40 plays a significant role in the renal autoregulatory response of preglomerular resistance vessels.

Renal Vascular Resistance and Aortic Pressure as Determinants of Sodium Reabsorption

1973 ◽  
Vol 51 (9) ◽  
pp. 654-664 ◽  
Author(s):  
S. M. Zweig ◽  
T. M. Daugharty ◽  
L. E. Earley
Keyword(s):  
Vascular Resistance ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Aortic Pressure ◽  
Renal Vascular Resistance ◽  
Sodium Reabsorption ◽  
Renal Perfusion Pressure ◽  
Bilateral Carotid ◽  
Infusion Of Norepinephrine ◽  
Renal Vascular

During induced renal vasodilatation, angiotensin and norepinephrine result in an increased excretion of sodium (UNaV), which has been attributed to transmission of elevated aortic pressure (PA) to peritubular capillaries and not to direct effects of the drugs on sodium reabsorption. The importance of PA, intrarenal hemodynamics, and other possible effects of angiotensin and norepinephrine was examined in anesthetized dogs in which one kidney was vasodilated by denervation or acetylcholine, and the opposite kidney served as control. During elevation of aortic pressure, following bilateral carotid occlusion and vagotomy (B.C.O. and V), infusion of angiotensin and norepinephrine, increased UNaV occurred on only the vasodilated side. Changes in UNaV on both sides are related inversely to renal vascular resistance (R.V.R.) before elevation PA, but not to changes in R.V.R., glomerular filtration rate (G.F.R.), or filtration fraction following elevation of PA. When renal perfusion pressure was controlled during aortic constriction, persistent increases in UNaV and urine flow rate were abolished during infusion of norepinephrine and after B.C.O. and V, and markedly reduced during infusion of angiotensin. These effects could not be attributed to changes in intrarenal hemodynamics. Thus increased sodium and water excretion following infusion of norepinephrine and angiotensin, and B.C.O. and V, can be largely attributed to an interplay of increased renal perfusion pressure and reduced preset renal vascular resistance.

Release by Vasopressin of E-Type Prostaglandins from the Rat Kidney

1977 ◽  
Vol 52 (1) ◽  
pp. 103-106
Author(s):  
C. Bell ◽  
M. K. K. Mya
Keyword(s):  
Smooth Muscle ◽  
Perfusion Pressure ◽  
Rat Kidney ◽  
Renal Perfusion ◽  
Prostaglandin Synthesis ◽  
Prostaglandin E ◽  
Receptor Stimulation ◽  
Renal Vasoconstriction ◽  
Renal Perfusion Pressure ◽  
Stimulation Of

1. In order to test whether the release of E-type prostaglandins from the kidney by various vasoconstrictor stimuli is related specifically to adrenoreceptor activation, we have compared release of prostaglandin E-like material from perfused rat kidneys during infusion of noradrenaline or vasopressin. 2. Concentrations of noradrenaline or vasopressin that produced comparable rises in renal perfusion pressure also released comparable amounts of prostaglandin E-like material. This effect was abolished by infusion of an inhibitor of prostaglandin synthesis into the kidney. 3. We conclude that liberation of E-type prostaglandins during renal vasoconstriction is probably related to the activation of intra-renal smooth muscle and does not involve any specific hormonal receptor. Stimulation of release of prostaglandin E may explain certain reported renal actions of vasopressin.

L-arginine improves transmission of perfusion pressure to the renal interstitium in Dahl salt-sensitive rats

1994 ◽  
Vol 266 (6) ◽  
pp. R1730-R1735 ◽  
Author(s):  
A. R. Patel ◽  
J. P. Granger ◽  
K. A. Kirchner
Keyword(s):  
Hydrostatic Pressure ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renal Capsule ◽  
Renal Perfusion Pressure ◽  
Renal Interstitium ◽  
Pressure Natriuresis ◽  
Acute Changes ◽  
The Relationship

L-Arginine normalizes pressure natriuresis in Dahl salt-sensitive (DS) rats. To determine the role of renal interstitial hydrostatic pressure (RIHP) in this phenomenon, we measured RIHP determined by servo-null during acute changes in renal perfusion pressure in anesthetized DS rats receiving L-arginine (300 mg.kg-1.day-1 ip) or vehicle for 3 wk. Dahl salt-resistant (DR) rats were controls. As observed previously, the slope of the pressure-natriuresis relationship was greater (P < 0.05) in L-arginine-treated DS rats than vehicle DS rats and not different from DR rats. The slope of the relationship between renal perfusion pressure and RIHP was greater (P < 0.05) in DR rats than vehicle DS rats. In L-arginine-treated DS rats the slope of this relationship was greater (P < 0.05) than that in vehicle DS rats and not different from DR rats. Removal of the renal capsule blunted the pressure-natriuresis relationship in L-arginine-treated DS rats but had no effect in vehicle DS rats. Thus L-arginine improves transmission of perfusion pressure into the renal interstitium in DS rats and may contribute to the improved pressure-natriuresis response.

Determinants of renal vasoconstriction after systemic inhibition of nitric oxide synthesis in rats

1996 ◽  
Vol 270 (6) ◽  
pp. R1203-R1207
Author(s):  
E. Brand-Schieber ◽  
M. Pucci ◽  
A. Nasjletti
Keyword(s):  
Nitric Oxide ◽  
Vascular Resistance ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renal Vascular Resistance ◽  
Tubuloglomerular Feedback ◽  
Nitric Oxide Synthesis ◽  
Renal Vasoconstriction ◽  
Renal Perfusion Pressure ◽  
Renal Vascular

The effects of NG-nitro-L-arginine (L-NNA, 10 mg/kg i.v.) on renal hemodynamics were examined in control rats, rats in which renal perfusion pressure was prevented from rising after L-NNA by constricting the abdominal aorta, and rats in which tubuloglomerular feedback was inhibited by furosemide pretreatment, ureteral ligation, or both interventions combined. In control rats, L-NNA increased (P < 0.05) renal vascular resistance (274 +/- 27%) along with systemic arterial (54 +/- 4%) and renal perfusion (54 +/- 5%) pressures and decreased (P < 0.05) renal blood flow (57 +/- 4%). In rats in which renal perfusion pressure was prevented from increasing along with systemic arterial pressure (54 +/- 4%), the L-NNA-induced elevation of renal vascular resistance (173 +/- 27%) was less intense (P < 0.05). In another study, where renal perfusion pressure was fixed at pre-L-NNA levels, L-NNA-induced increases in renal vascular resistance (130 +/- 20%) were attenuated (P < 0.05) further with furosemide pretreatment (52 +/- 12%), with ureteral ligation (75 +/- 10%), and with furosemide pretreatment and ureteral ligation combined (32 +/- 8%). These data suggest that vasoconstrictor mechanisms linked to tubuloglomerular feedback and perfusion pressure elevation contribute to renal vasoconstriction after systemic inhibition of nitric oxide synthesis with L-NNA.

Blood flow-dependent changes in renal interstitial guanosine 3′,5′-cyclic monophosphate in rabbits

2002 ◽  
Vol 282 (2) ◽  
pp. F238-F244 ◽  
Author(s):  
Akira Nishiyama ◽  
Shoji Kimura ◽  
Toshiki Fukui ◽  
Matlubur Rahman ◽  
Hirohito Yoneyama ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Perfusion Pressure ◽  
Ambient Pressure ◽  
Renal Perfusion ◽  
Cyclic Monophosphate ◽  
Renal Perfusion Pressure ◽  
Highly Correlated ◽  
Acute Changes ◽  
Oxide Synthase

We examined responses of renal interstitial guanosine 3′,5′-cyclic monophosphate (cGMP) to changes in renal perfusion pressure (RPP) within and below the range of renal blood flow (RBF) autoregulation. A microdialysis method was used to monitor renal cortical and medullary interstitial cGMP levels in anesthetized rabbits. RPP was reduced in two steps: from ambient pressure (89 ± 3 mmHg) to 70 ± 2 mmHg ( step 1) and then to 48 ± 3 mmHg ( step 2). RBF was maintained in step 1 but was significantly decreased in step 2 from 2.94 ± 0.23 to 1.47 ± 0.08 ml · min−1 · g−1. Basal interstitial concentrations of cGMP were significantly lower in the cortex than in the medulla (12.1 ± 1.4 and 19.9 ± 0.4 nmol/l, respectively). Cortical and medullary cGMP did not change in step 1 but were significantly decreased in step 2, with significantly less reduction in cGMP concentrations in the medulla than in the cortex (−25 ± 3 and −44 ± 3%, respectively). Over this pressure range, changes in cortical and medullary cGMP were highly correlated with changes in RBF ( r= 0.94, P < 0.005 for cortex; r = 0.82, P < 0.01 for medulla). Renal interstitial nitrate/nitrite was not changed in step 1 but was significantly decreased in step 2 (−38 ± 2% in cortex and −20 ± 2% in medulla). Nitric oxide synthase inhibition with N G-nitro-l-arginine methyl ester (l-NAME, 30 mg/kg bolus, 50 mg · kg−1 · h−1 iv infusion) significantly decreased RBF (by −46 ± 4%) and interstitial concentrations of cGMP (−27 ± 4% in cortex and −22 ± 4% in medulla, respectively). During l-NAME treatment, renal interstitial concentrations of cGMP in the cortex and medulla were similarly not altered in step 1. However, l-NAME significantly attenuated cGMP responses to a reduction in RPP in step 2. These results indicate that acute changes in RBF result in alterations in nitric oxide-dependent renal interstitial cGMP levels, with differential effects in the medulla compared with the cortex.

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