Hormonal control of kidney functions at the cell level.

Morel, François M. M.; Doucet, Alain

doi:10.1152/physrev.1986.66.2.377

Cited by 199 publications

(96 citation statements)

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“…The catheter was flushed with saline after sampling. The samples were taken at rest, 30, 60 and 90 min in the HST, and at the same times on days one and five of the acclimation regimes, but with the omission of the 30 min sample (Morel and Doucet 1986;Creasy 2002 (Ramanathan 1964) and b T = 0.9 T re + 0.1 T sk . Temperatures were logged at 60-s intervals (1200 series, Squirrel Grant Instruments, Cambridge, England).…”

Section: Fluid Regulatory and Stress Hormonesmentioning

confidence: 99%

Induction and decay of short-term heat acclimation

et al. 2009

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Abstract:Most advice for heat adaptation is to use long-term (>10 d) regimes, in which hydration status is maintained. We tested the hypothesis that short-term (5-day) heat acclimation would confer substantial improvements in physiological strain and exercise tolerance for exercise in the heat, and fluid regulatory strain provides a thermally-independent stimulus for such adaptations. Ten moderately-fit males were heat acclimated using controlled hyperthermia (rectal temperature 38.5°C) for 90 min on five consecutive days (T a = 40°C, 60% RH), on two occasions separated by a five-week washout, in a randomly assigned, cross-over design; one with euhydration (EUH) and one with dehydration (DEH) during acclimation bouts. One week before, then on the 2 nd day after each acclimation regime, a heat stress test (HST) was completed, comprising cycling at 40% peak power output for 90 min (T a = 35°C, 60% RH), before incrementing to exhaustion. Plasma volume (PV) at rest was measured using CO rebreathing. Acclimation exercise-induced response of[aldo] p became more pronounced across DEH (  178 pg . mL -1 ; 95%CI: 33 to 324) but not EUH (  -47 pg . mL -1 : -209 to 115) and this difference was significant (P=0.02).Compared to EUH, permissive DEH during acclimation bouts conferred larger acclimation-induced increases in resting PV (4.1%: -1.5 to 9.8%; P=0.06), F Q  (4.2: 0.7 to 7.8 ml . min -1. 100 ml -1 ; P=0.009), FVC (0.06: 0.02 to 0.10 ml . 100ml Tissue -1. min -1. mmHg -1 ; P=0.006) and decreased end-exercise c f by 17% (19: -29 to 9 b·min-1; P=0.05). In conclusion, short-term (5-day) heat acclimation was effective with several adaptations more pronounced after fluid-regulatory strain from a dehydration acclimation regime.

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Section: Fluid Regulatory and Stress Hormonesmentioning

confidence: 99%

Induction and decay of short-term heat acclimation

et al. 2009

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“…These respond to the action of aldosterone by induction of RNA synthesis prior to the exchange of Na+ with K+ and protons. Aldosteroneinduced changes also occur in the activity of peritubular Na,K-ATPase as well as in a number of mitochondrial enzymes involved in both ATP synthesis and the tricarboxylic acid cycle (Morel & Doucet, 1986). With the close chemical similarities of spironolactone and canrenoate to aldosterone, the mineralocorticoid receptor is the likely endogenous ligand for these antikaliuretic diuretics (Feldman, 1978).…”

Section: Intrarenal Effectsmentioning

confidence: 99%

Evolution of diuretics and ACE inhibitors, their renal and antihypertensive actions‐parallels and contrasts.

Lant

1987

Brit J Clinical Pharma

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1 The emergence of diuretic drugs and angiotensin converting enzyme (ACE) inhibitors ranks amongst the major therapeutic advances of modern medicine. The discovery of these drug groups arose largely by chance, yet each has dramatically influenced the treatment of congestive cardiac failure and arterial hypertension. 2 The central role which diuretics have had in the management of both oedema and hypertension hinges on their ability to induce a net renal excretion of solute and water by selective interference with either active or passive ion transport processes in different segments of the nephron. Irrespective of sites of action, the continued antihypertensive action of diuretics is characterized by a reduction in plasma volume and extracellular fluid (ECF) volume that lasts for as long as the diuretic is given. The mechanism of this effect remains unclear but may involve autoregulatory reactions that leave cardiac output unaltered but maintain a sustained reduction in total peripheral resistance. 3 ACE inhibitors also lower blood pressure by decreasing total peripheral resistance, leaving cardiac output, plasma volume and ECF volume unchanged. The detailed way these haemodynamic changes are achieved remains unknown but inhibition of converting enzyme present not only in the kidney but also in many extrarenal tissue sites, appears important. In both hypertension and cardiac failure, however, the kidney acts as a key target organ for ACE inhibitors. The increased renal vascular resistance and inappropriate renal salt excretion are reversed with enhanced renal blood flow and saluresis. Both angiotensin II (All) and vasopressin-mediated contraction of glomerular mesangial cells is inhibited, making glomerular filtration more efficient. Reduced aldosterone secondary to blockade of AII formation contributes to saluresis whilst encouraging positive potassium balance. ACE inhibition also impairs breakdown of kinins which may contribute to intrarenal and peripheral vasodilation either on their own or via release of prostaglandins and other vasoactive substances.4 The hypotensive actions of diuretics are potentiated by ACE inhibition primarily through blockade of AII formation and prevention of secondary aldosteronism. In combination, these drugs permit low doses to be used because of their synergistic effects. 5 Caution has to be exercised whenever ACE inhibition is used, without and especially with diuretics, in the management of renovascular hypertension and other low-perfusion states. In these circumstances, AII plays an important autoregulatory role in preserving glomerular filtration through an increase in post-glomerular resistance. Suppression of angiotensin formation with an ACE inhibitor can cause a critical reduction in glomerular perfusion. On the other hand, with careful titration, the dual actions of low-dose loop diuretics and an ACE inhibitor may be highly efficacious in treating severe heart failure and totally prevent such serious metabolic sequelae as azotaemia and hyponatraemia. 6 Unlike the experien...

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“…As previously discussed, di erent experimental results support the conclusion that adenylyl cyclase activity is stimulated by AVP and glucagon in principal cells and intercalated cells, respectively (Morel & Doucet, 1986;ChabardeÁ s et al, 1996). In rat MTAL, there is only one morphological cell type (Madsen & Tisher, 1986) and di erent hormones including AVP and glucagon stimulate the same catalytic units of adenylyl cyclase (Morel et al, 1987).…”

Section: Introductionmentioning

confidence: 59%

“…A similar e ect of PGE 2 has been previously observed in the isoproterenol-sensitive cells of rat CCD (ChabardeÁ s et al, 1990). Glucagon-and isoproterenol-stimulated cyclic AMP synthesis are located in intercalated cells which are involved in proton secretion and/or bicarbonate reabsorption (Madsen & Tisher, 1986;Morel & Doucet, 1986). These observations therefore support a regulatory role of PGE 2 in the control of acid-base balance, in addition to its well known inhibitory e ect on the urinary concentration processes (Stokes, 1981).…”

Section: Discussionmentioning

confidence: 99%

“…The urinary concentration process is regulated by arginine vasopressin (AVP) which increases intracellular adenosine 3':5' cyclic monophosphate (cyclic AMP) in two well-de®ned segments of the rat renal tubule, the thick ascending limb and the collecting tubule (Morel & Doucet, 1986). Previous studies on rat microdissected segments have established that the AVPdependent cyclic AMP accumulation can be decreased by prostaglandin E 2 (Torikai & Kurokawa, 1983;ChabardeÁ s et al, 1990;Aarab et al, 1993;Firsov et al, 1995;De Jesus Ferreira et al, 1998).…”

Section: Introductionmentioning

confidence: 99%

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Cell‐specific coupling of PGE₂ to different transduction pathways in arginine vasopressin‐ and glucagon‐sensitive segments of the rat renal tubule

Aarab

Siaume-Perez

Chabardès

1999

British J Pharmacology

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1 The aim of the present study was to investigate the transduction pathways elicited by prostaglandin E 2 (PGE 2 ) to inhibit hormone-stimulated adenosine 3':5'-cyclic monophosphate (cyclic AMP) accumulation in the outer medullary collecting duct (OMCD) and medullary thick ascending limb (MTAL) microdissected from the rat nephron. 2 In the OMCD, 0.3 mM PGE 2 and low concentrations of Ca 2+ ionophores (10 nM ionomycin or 50 nM A23187) inhibited by about 50% a same pool of arginine vasopressin (AVP)-stimulated cyclic AMP content through a same process insensitive to Bordetella pertussis toxin (PTX). 3 Sulprostone, an agonist of the EP 1 /EP 3 subtypes of the PGE 2 receptor, decreased AVPdependent cyclic AMP accumulation in OMCD and MTAL samples. The concentration eliciting half-maximal inhibition was of about 50 nM in OMCD and 0.1 nM in MTAL. 4 In MTAL, 1 nM sulprostone and PGE 2 inhibited by about 90% a same pool of AVP-dependent cyclic AMP content through a PTX-sensitive, Ca 2+ -independent pathway. 5 In the OMCD, PGE 2 decreased by about 50% glucagon-dependent cyclic AMP synthesis by a process sensitive to PTX and Ca 2+ -independent. Sulprostone 1 nM induced the same level of inhibition. 6 These results demonstrate that PGE 2 decrease hormone-dependent cyclic AMP accumulation through a Gai-mediated inhibition of adenylyl cyclase activity in MTAL cells and glucagon-sensitive cells of the OMCD or through a PTX-insensitive increase of intracellular Ca 2+ concentration in AVP-sensitive cells of the OMCD.

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Hormonal control of kidney functions at the cell level.

Cited by 199 publications

References 0 publications

Induction and decay of short-term heat acclimation

Induction and decay of short-term heat acclimation

Evolution of diuretics and ACE inhibitors, their renal and antihypertensive actions‐parallels and contrasts.

Cell‐specific coupling of PGE₂ to different transduction pathways in arginine vasopressin‐ and glucagon‐sensitive segments of the rat renal tubule

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Hormonal control of kidney functions at the cell level.

Cited by 199 publications

References 0 publications

Induction and decay of short-term heat acclimation

Induction and decay of short-term heat acclimation

Evolution of diuretics and ACE inhibitors, their renal and antihypertensive actions‐parallels and contrasts.

Cell‐specific coupling of PGE2 to different transduction pathways in arginine vasopressin‐ and glucagon‐sensitive segments of the rat renal tubule

Contact Info

Product

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Cell‐specific coupling of PGE₂ to different transduction pathways in arginine vasopressin‐ and glucagon‐sensitive segments of the rat renal tubule