alpha<sub>2</sub>-Adrenoceptor Regulation of Parathyroid Hormone Function in the Isolated Perfused Kidney

Jeffries, William B.; Dreal, P Van; Pettinger, William A.

doi:10.3109/10641968909045419

Cited by 3 publications

(2 citation statements)

References 15 publications

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“…Although the physiological role of renal a2 adrenoceptors remains to be fully established, they have been reported to constrict (11)(12)(13) or relax (2) the renal vasculature, suppress renin secretion (14,15), and stimulate reabsorption ofsodium from the proximal nephron by stimulating Na/H exchange (16)(17)(18) and from the loop ofHenle by suppressing furosemide- (19) or prostaglandin-(20) mediated increases in cAMP. a2 Receptors also inhibit reabsorption of salt and water from the distal nephron by antagonizing the effects of vasopressin (21)(22)(23)(24)(25) and potentiating the effect ofatrial natriuretic peptide (26).…”

Section: Discussionmentioning

confidence: 99%

“…a2 Receptors also inhibit reabsorption of salt and water from the distal nephron by antagonizing the effects of vasopressin (21)(22)(23)(24)(25) and potentiating the effect ofatrial natriuretic peptide (26). In many of these cases, a2 adrenoceptors function by modulating the activity of other effector systems (16)(17)(18)(27)(28)(29)(30)(31)(32)(33). In situations where a2 receptors modulate the influence of multiple effectors, the physiological outcome of a2 receptor stimulation or blockade will depend upon the previous activities of potentially competing systems that are individually conditioned by interactions with a2 adrenoceptors.…”

Section: Discussionmentioning

confidence: 99%

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Interaction between alpha 2-adrenergic and angiotensin II systems in the control of glomerular hemodynamics as assessed by renal micropuncture in the rat.

Thomson

Gabbai²,

Tucker³

et al. 1992

J. Clin. Invest.

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The hypothesis that renal a2 adrenoceptors influence nephron filtration rate (SNGFR) via interaction with angiotensin II (All) was tested by renal micropuncture. The physical determinants of SNGFR were assessed in adult male Munich Wistar rats 5-7 d after ipsilateral surgical renal denervation (DNX). DNX was performed to isolate inhibitory central and presynaptic a2 adrenoceptors from end-organ receptors within the kidney. Two experimental protocols were employed: one to test whether prior All receptor blockade with saralasin would alter the glomerular hemodynamic response to a2 adrenoceptor stimulation with the selective agonist B-HT 933 under euvolemic conditions, and the other to test whether B-HT 933 would alter the response to exogenous All under conditions of plasma volume expansion. In euvolemic rats, B-HT 933 caused SNGFR to decline as the result of a decrease in glomerular ultrafiltration coefficient (LpA), an effect that was blocked by saralasin. After plasma volume expansion, B-HT 933 showed no primary effect on LpA but heightened the response of arterial blood pressure, glomerular transcapillary pressure gradient, and LpA to All. The parallel results of these converse experiments suggest a complementary interaction between renal a2-adrenergic and All systems in the control of LpA. (J. Clin. Invest. 1992.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Interaction between alpha 2-adrenergic and angiotensin II systems in the control of glomerular hemodynamics as assessed by renal micropuncture in the rat.

Thomson

Gabbai²,

Tucker³

et al. 1992

J. Clin. Invest.

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Effects of PTH(1-34) on Blood Pressure, Renal Function, and Hormones in Essential Hypertension The Altered Pattern of Reactivity May Counteract Raised Blood Pressure

Jespersen

Randløv

Abrahamsen

et al. 1997

American Journal of Hypertension

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As it has been suggested that parathyroid hormone (PTH) is implicated in the pathophysiology of essential hypertension, the effects of PTH(1-34) were assessed during infusion over 120 min in ten men with essential hypertension and in ten healthy men. Ionized calcium was kept constant by a clamping technique. Mean arterial blood pressure fell slightly in the patients (116 mm Hg, median, before, and 108 mm Hg during the infusion, P < .01), but remained unchanged in the controls (median 87 mm Hg). The pulse rate rose to a similar extent in the two groups, but cardiac output, measured by the CO2 rebreathing technique, was unchanged. The glomerular filtration rate (GFR) was slightly lower in the hypertensives than in the controls at baseline (92 v 109 mL/min, P < .02), but it increased similarly during PTH infusion in both groups (+13% v +9%, medians), as did the effective renal plasma flow (+50% v +38%). The urinary rate of sodium excretion, which was similar at baseline, increased more in the patients than in the controls (+191% v +46%, P < .05); this was mainly attributable to a reduction in the tubular reabsorption of sodium. Calculations based on lithium clearance indicated that mainly the proximal tubular reabsorption of sodium decreased during PTH infusion. Baseline plasma PTH(1-84) was higher in the patients than in the controls (20.5 ng/L v 16.5 ng/L, P < .05). The baseline plasma values of renin, aldosterone, atrial natriuretic peptide, endothelin, and noradrenaline were similar in the two groups. During infusion of PTH, renin increased less in the patients than in the controls (P < .02), and aldosterone increased only in the controls (P < .01). The other hormonal values remained unchanged. In conclusion, the patients with essential hypertension had increased baseline PTH values, but nevertheless PTH had more marked vasodilative and natriuretic effects than in the controls. PTH thus seems to counteract rather than aggravate elevation of blood pressure in these patients.

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Na(+)-H+ exchanger subtypes: a predictive review

Clark

Limbird

1991

American Journal of Physiology-Cell Physiology

143

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In recent years, many reports have appeared describing distinct heterogeneity of proteins that heretofore were considered to be a single species or type. The division of proteins into different classes or subtypes is aided by pharmacological tools such as selective ligands, functional measurements such as those examining kinetic or regulatory differences, and molecular biological approaches that have identified distinct genes coding for similar yet distinguishable gene products. Currently, much effort is directed toward understanding the significance of these sometimes subtle differences in terms of functional consequences for the cells in which they exist. Although most reports to date involve hormone and neurotransmitter receptor subtypes, it is also possible that other cell surface molecules such as ion transporters exist as multiple subtypes. In this paper we review the current evidence that Na(+)-H+ exchange activity is mediated by different Na(+)-H+ exchanger subtypes. Although subtypes have not been identified with certainty, we can predict certain distinguishing characteristics that these putative subtypes may have that may be of value in correlating predicted gene products obtained from cDNA cloning with previously characterized Na(+)-H+ exchangers.

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alpha₂-Adrenoceptor Regulation of Parathyroid Hormone Function in the Isolated Perfused Kidney

Cited by 3 publications

References 15 publications

Interaction between alpha 2-adrenergic and angiotensin II systems in the control of glomerular hemodynamics as assessed by renal micropuncture in the rat.

Interaction between alpha 2-adrenergic and angiotensin II systems in the control of glomerular hemodynamics as assessed by renal micropuncture in the rat.

Effects of PTH(1-34) on Blood Pressure, Renal Function, and Hormones in Essential Hypertension The Altered Pattern of Reactivity May Counteract Raised Blood Pressure

Na(+)-H+ exchanger subtypes: a predictive review

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alpha2-Adrenoceptor Regulation of Parathyroid Hormone Function in the Isolated Perfused Kidney

Cited by 3 publications

References 15 publications

Interaction between alpha 2-adrenergic and angiotensin II systems in the control of glomerular hemodynamics as assessed by renal micropuncture in the rat.

Interaction between alpha 2-adrenergic and angiotensin II systems in the control of glomerular hemodynamics as assessed by renal micropuncture in the rat.

Effects of PTH(1-34) on Blood Pressure, Renal Function, and Hormones in Essential Hypertension The Altered Pattern of Reactivity May Counteract Raised Blood Pressure

Na(+)-H+ exchanger subtypes: a predictive review

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alpha₂-Adrenoceptor Regulation of Parathyroid Hormone Function in the Isolated Perfused Kidney