α1-Adrenoceptor subtypes mediating antinatriuresis in Wistar and stroke-prone spontaneously hypertensive rats

doi:10.1016/0014-2999(95)00637-0

European Journal of Pharmacology

Volume 294, Issues 2–3, 29 December 1995, Pages 727-736

https://doi.org/10.1016/0014-2999(95)00637-0 Get rights and content

Abstract

This study examined the α₁-adrenoceptor subtypes involved in mediating adrenergically induced Na⁺ reabsorption in the kidney of pentobarbitone anaesthetised Wistar and stroke-prone spontaneously hypertensive rats (SHRSP). Close renal-arterial phenylephrine (50–100 μg kg⁻¹ h⁻¹) administration in Wistars, with regulated renal perfusion pressure, caused small reductions in renal haemodynamics but large reductions, of 35%, 64% and 57% (all P < 0.05), in urine volume, absolute and fractional Na⁺ excretions. The magnitude of these excretory responses to phenylephrine were similar in the presence of the α_1B-adrenoceptor alkylating agent, chloroethylclonidine (10 μg kg⁻¹ h⁻¹), but were blocked during administration of the α_1A-adrenoceptor antagonist, 5-methylurapidil (10 μg kg⁻¹ h⁻¹). Phenylephrine infusion in the stroke-prone spontaneously hypertensive rats caused changes in renal haemodynamics and fluid excretion of comparable magnitude to that achieved in Wistars which was blocked by 5-methylurapidil but not chloroethylclonidine. These observations suggest that in Wistar and stroke-prone spontaneously hypertensive rats the adrenergically induced Na⁺ reabsorptive responses are mediated by α_1A-adrenoceptors.

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Cited by (17)

Autonomic regulation of kidney function
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Citation Excerpt :
Later reports which attempted to examine in greater depth the subtypes of α1-adrenoceptors involved in meditating the renal nerve-induced reductions in renal hemodynamics found that a large component required activation of the α1A-adrenoceptor subtype (Witkowski et al., 2011). At the level of the tubular epithelia cells, a number of studies provided evidence that the antinatriuresis resulting from low-level stimulation of the renal sympathetic nerves could be blocked by prazosin, but not by the α2-adrenoceptor antagonist idazoxan, consistent with the involvement of α1-adrenoceptors (Johns and Manitius, 1986) which was later shown (Sattar and Johns, 1995) to primarily involve α1A-adrenoceptors. It became evident at a very early stage that renal nerve-dependent renin release involved the activation of β-adrenoceptors.
The kidneys play a central role in cardiovascular homeostasis by ensuring a balance between the fluid taken in and that lost and excreted during everyday activities. This ensures stability of extracellular fluid volume and maintenance of normal levels of blood pressure. Renal fluid handling is controlled via neural and humoral influences, with the former determining a rapid dynamic response to changing intake of sodium whereas the latter cause a slower longer-term modulation of sodium and water handling. Activity in the renal sympathetic nerves arises from an integration of information from the high and low pressure cardiovascular baroreceptors, the somatosensory and visceral systems as well as the higher cortical centers. Each sensory system provides varying input to the autonomic centers of the hypothalamic and medullary areas of the brain at a level appropriate to the activity being performed. In pathophysiological states, such as hypertension, heart failure and chronic renal disease, there may be an inappropriate sympathoexcitation causing sodium retention which exacerbates the disease process. The contribution of the renal sympathetic nerves to these cardiovascular diseases is beginning to be appreciated with the demonstration that renal denervation of resistant hypertensive patients results in a long-term normalization of blood pressure.
Vascular α(1D)-adrenoceptors: Are they related to hypertension?
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Heterogeneity of vascular α₁-adrenoceptor subtypes has been revealed by pharmacological and molecular biology studies (i.e., α_1A- , α_1B- , and α_1D-adrenoceptors). The α_1D-adrenoceptor subtype is predominantly involved in the contraction of a variety of vessels and its role in the control of blood pressure has been suggested, a phenomenon probably related to aging. Recent advances in the use of young pre-hypertensive rats and adult spontaneously hypertensive rats with one kidney and Grollman-type renal hypertension suggest vascular α_1D-adrenoceptor involvement in the increased blood pressure. The possible role of α_1D-adrenoceptors in the genesis/maintenance of hypertension is discussed in this review.
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Regular paperα1-Adrenoceptor subtypes mediating antinatriuresis in Wistar and stroke-prone spontaneously hypertensive rats

Abstract

Eur. J. Pharmacol.

Eur. J. Pharmacol.

Comp. Biochem. Physiol.

The α-adrenoceptor mediating the tubular actions of the renal nerves in spontaneously hypertensive and stroke-prone spontaneously hypertensive rats

J. Auton. Pharmacol.

The characteristics of alpha-adrenoceptors mediating the renal nerve induced antinatriuresis and antidiuresis in hypertensive rats

J. Hypertens.

Innervation of renal cortical tubules, a quantative study

Am. J. Physiol.

Acute unilateral denervation in rats with extracellular volume expansion

Am. J. Physiol.

A method for determination of inulin in plasma and urine

Acta Physiol. Scand.

Effects of renal nerves in NaCl and H2O transport in Henle's loop of the rat

Am. J. Physiol.

Renal alpha-adrenergic receptor abnormality in the spontaneously hypertensive rat

Hypertension

Heterogeneity of α1-adrenergic receptors revealed by chloroethylclonidine

Mol. Pharmacol.

α1-adrenoceptors linked to different mechanisms for increasing intracellular calcium in smooth muscle

Nature

Regular paper
α₁-Adrenoceptor subtypes mediating antinatriuresis in Wistar and stroke-prone spontaneously hypertensive rats

Effects of renal nerves in NaCl and H₂O transport in Henle's loop of the rat

Heterogeneity of α₁-adrenergic receptors revealed by chloroethylclonidine

α₁-adrenoceptors linked to different mechanisms for increasing intracellular calcium in smooth muscle