Mechanism of renin release in exercising dog

Zambraski, Edward J.; Tucker, MA; Lakas, C. S.; Grassl, Steven M.; Scanes, Colin G.

doi:10.1152/ajpendo.1984.246.1.e71

Cited by 15 publications

(12 citation statements)

References 18 publications

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“…The increased peripheral noradrenergic activation observed in Dh might result in part from the reduced PV which could stimulate cardiopulmonary barore¯exes because of the expected reductions in cardiac ®lling pressure, and stroke volume as re¯ected by the higher values of HR that occur during exercise (Fortney et al 1983;Nielsen et al 1990). Elevated sympathetic activity has also been shown to be responsible for renin release during exercise in both animals (Zambraski et al 1984) and humans (Kjaer et al 1995). In our study, a highly signi®cant relationship was observed between the changes from resting levels in plasma renin and NA during exercise in C and Dh (r = 0.77, P < 0.001).…”

Section: Discussionsupporting

confidence: 61%

Effects of hydration state on hormonal and renal responses during moderate exercise in the heat

Melin

Jimenez

Savourey

et al. 1997

European Journal of Applied Physiology

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The effects of hydromineral hormones and catecholamines on renal concentrating ability at different hydration states were examined in five male volunteers while they performed three trials. Each of these trials comprised a 60-min exercise bout on a treadmill (at 50% of maximal oxygen uptake) in a warm environment (dry bulb temperature, 35 degrees C; relative humidity, 20-30%). In one session, subjects were euhydrated before exercise (C). In the two other sessions, after thermal dehydration (loss of 3% body mass) which markedly reduced plasma volume (PV) and increased plasma osmolality (osm[pl]), the subjects exercised either not rehydrated (Dh) or rehydrated (Rh) by drinking 600 ml of mineral water before and 40 min after the onset of exercise. During exercise in the Dh compared to C state, plasma renin, aldosterone, arginine vasopressin (AVP), noradrenaline and adrenaline concentrations were increased (P < 0.05). A reduction in creatinine clearance and urine flow was also observed (P < 0.05) together with a decrease in urine osmolality, osmolar clearance and sodium excretion, while free water clearance increased (P < 0.05). However, compared to Dh, Rh partially restored PV and osm(pl) and induced a marked reduction in the time courses of both the plasma AVP and catecholamine responses (P < 0.05). Values for renal water and electrolyte excretion were intermediate between those of Dh and C. Plasma atrial natriuretic peptide presented similar changes whatever the hydration state. These results demonstrate that during moderate exercise in the heat, renal concentrating ability is paradoxically reduced by prior dehydration in spite of high plasma AVP levels, and might be the result of marked activation of the sympatho-adrenal system. Rehydration, by reducing this activation, could partially restore the renal concentrating ability despite the lowered plasma AVP.

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Section: Discussionsupporting

confidence: 61%

Effects of hydration state on hormonal and renal responses during moderate exercise in the heat

Melin

Jimenez

Savourey

et al. 1997

European Journal of Applied Physiology

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“…The exercise-induced increase in PRC is mediated mainly by stimulation of β " -adrenergic receptors [28]. In line with previous studies [26][27][28], the present decrease in PRC caused by indomethacin did not prevent exercise-induced increases in PRC and PAC, indicating that this response does not depend on changes in renal prostaglandin synthesis.…”

Section: Discussionsupporting

confidence: 90%

Non-steroidal anti-inflammatory drugs and renal response to exercise: a comparison of indomethacin and nabumetone

Olsen¹,

JENSEN²,

HANSEN³

et al. 1999

Clinical Science

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Nabumetone, a newer non-steroidal anti-inflammatory drug (NSAID) which preferentially blocks cyclo-oxygenase-2 activity, may be less nephrotoxic than indomethacin. This study tested whether nabumetone has effects different from those of indomethacin on exercise-induced changes in renal function and the renin-aldosterone system. In a randomized fashion, ten subjects were studied after indomethacin (100 mg), nabumetone (1 g) or no medication (control) administered orally at 22.00 hours on the day before each study day, and again at 8.00 hours upon arrival at the laboratory. Renal function was studied at baseline, during graded 20-min exercise sessions at 25%, 50% and 75% of the maximal oxygen uptake rate, and subsequently during two 1-h recovery periods. Heart rate, arterial blood pressure, cardiac output and plasma catecholamines at rest and during exercise were not altered by indomethacin or nabumetone. Indomethacin decreased urinary rates of excretion of 6-oxo-prostaglandin F(1alpha) (6-oxo-PGF(1alpha)) and thromboxane B(2) in all study periods. Nabumetone decreased 6-oxo-PGF(1alpha) excretion during and after exercise. Excretion rates for PGE(2) did not change. Neither indomethacin nor nabumetone changed baseline values or exercise-induced decreases in renal plasma flow or glomerular filtration rate. Indomethacin, but not nabumetone, decreased sodium excretion, urine flow rate and free water clearance. The renal response to exercise, however, remained unchanged. In contrast with nabumatone, indomethacin decreased the plasma renin concentration. Thus, during exercise, nabumetone may decrease the excretion of 6-oxo-PGF(1alpha) by inhibition of cyclo-oxygenase-1 or by inhibition of specific exercise-induced activation of cyclo-oxygenase-2, or both. None of the drugs changed the renal response to exercise. Inhibition by indomethacin of angiotensin II and thromboxane A(2) synthesis may, during exercise, counterbalance renal vasoconstriction caused by blockade of vasodilatory prostaglandins.

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“…1). It has been shown in dogs that similar regimens of metoprolol administration (0.5-2.0 mg/kg iv or 0.5-2.0 g⅐kg Ϫ1 ⅐min Ϫ1 into the renal artery) abolishes the increase in renin secretion associated with low level renal nerve stimulation (17,20), administration of the ␤ 1-adrenoceptor agonist prenalterol (21), and exercise (43).…”

Section: Animalsmentioning

confidence: 99%

Normotensive sodium loading in conscious dogs: regulation of renin secretion during β-receptor blockade

Bie¹,

Mölström²,

Wamberg³

2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Renin secretion is regulated in part by renal nerves operating through beta1-receptors of the renal juxtaglomerular cells. Slow sodium loading may decrease plasma renin concentration (PRC) and cause natriuresis at constant mean arterial blood pressure (MAP) and glomerular filtration rate (GFR). We hypothesized that in this setting, renin secretion and renin-dependent sodium excretion are controlled by via the renal nerves and therefore are eliminated or reduced by blocking the action of norepinephrine on the juxtaglomerular cells with the beta1-receptor antagonist metoprolol. This was tested in conscious dogs by infusion of NaCl (20 micromol.kg(-1).min(-1) for 180 min, NaLoad) during regular or low-sodium diet (0.03 mmol.kg(-1).day(-1), LowNa) with and without metoprolol (2 mg/kg plus 0.9 mg.kg(-1).h(-1)). Vasopressin V2 receptors were blocked by Otsuka compound OPC31260 to facilitate clearance measurements. Body fluid volume was maintained by servocontrolled fluid infusion. Metoprolol per se did not affect MAP, heart rate, or sodium excretion significantly, but reduced PRC and ANG II by 30-40%, increased plasma atrial natriuretic peptide (ANP), and tripled potassium excretion. LowNa per se increased PRC (+53%), ANG II (+93%), and aldosterone (+660%), and shifted the vasopressin function curve to the left. NaLoad elevated plasma [Na+] by 4.5% and vasopressin by threefold, but MAP and plasma ANP remained unchanged. NaLoad decreased PRC by approximately 30%, ANG II by approximately 40%, and aldosterone by approximately 60%, regardless of diet and metoprolol. The natriuretic response to NaLoad was augmented during metoprolol regardless of diet. In conclusion, PRC depended on dietary sodium and beta1-adrenergic control as expected; however, the acute sodium-driven decrease in PRC at constant MAP and GFR was unaffected by beta1-receptor blockade demonstrating that renin may be regulated without changes in MAP, GFR, or beta1-mediated effects of norepinephrine. Low-sodium diet augments vasopressin secretion, whereas ANP secretion is reduced.

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Mechanism of renin release in exercising dog

Cited by 15 publications

References 18 publications

Effects of hydration state on hormonal and renal responses during moderate exercise in the heat

Effects of hydration state on hormonal and renal responses during moderate exercise in the heat

Non-steroidal anti-inflammatory drugs and renal response to exercise: a comparison of indomethacin and nabumetone

Normotensive sodium loading in conscious dogs: regulation of renin secretion during β-receptor blockade

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