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

Abstract

1. Experiments were undertaken in groups of pentobarbitone anaesthetized normotensive, spontaneously hypertensive or stroke-prone spontaneously hypertensive rats to determine the alpha-adrenoceptor subtype mediating renal nerve-stimulated tubular sodium readsorption at the level of the nephron. 2. In normotensive rats, stimulation of the renal nerves at low frequencies, which caused small changes in renal blood flow and glomerular filtration rate, caused significant reductions in urine volume, absolute sodium excretion and fractional sodium excretion of between 35 and 55% (P less than 0.01) respectively. The renal nerve-mediated antidiuresis and antinatriuresis were inhibited by the administration of doses of prazosin which selectively blocked alpha 1-adrenoceptor vascular responses. The magnitude of the renal nerve-induced excretory responses was unaffected by the presence of idazoxan at a dose which selectively blocked alpha 2-adrenoceptor blood pressure and renal vasoconstrictor responses. 3. Renal nerve stimulation in spontaneously hypertensive rats caused small falls in renal blood flow and glomerular filtration rate but larger significant reductions in urine flow, absolute and fractional sodium excretions of between 40 and 50%, which were of similar magnitude to those observed in the normotensive rats. The renal nerve-induced reductions in urine flow, absolute and fractional sodium were abolished in the presence of prazosin but were unaffected by idazoxan. 4. In the stroke-prone spontaneously hypertensive rat, low level renal nerve stimulation had small effects on renal haemodynamics but reduced urine flow, absolute and fractional sodium excretions by similar magnitudes to those in the other groups of rats, by between 45 and 55%. These renal nerve-induced reductions in water and sodium excretion were abolished by prazosin but not by idazoxan. 5. Together, these data show that in both normotensive rats and the two models of genetic hypertension, the renal nerves have important actions on the renal tubules to increase sodium and water reabsorption while having little effect on renal haemodynamics. In all these groups of rats this tubular action of the renal nerves was mediated by alpha 1- but not alpha 2-adrenoceptors.

Renal effects of neuropeptide Y

“…Sympathetic stimulation may inhibit urine formation, and this may be due predominantly to the action of noradrenaline on tubular α-adrenoceptors [3]. Stimulation of prejunctional NPY receptors in a variety of tissues and species potently inhibits noradrenaline release from sympathetic nerve terminals [34].…”

Ontogenesis of sympathetic responsiveness in spontaneously hypertensive rats. I. Renal alpha 1-, alpha 2-, and beta-adrenergic receptors and their signaling.

“…This idea is further supported by recent data demonstrating that the reductions in urine formation and fractional and absolute sodium excretion caused by renal nerve stimulation and mediated by a,-adrenergic receptors 9 are similar in extent in WKY rats and SHR. 37 Moreover, continuous treatment with the a,-adrenergic antagonist terazosin has been demonstrated not to prevent the development of hypertension in SHR. 38 On the other hand, increased afferent and efferent arteriolar vasoconstrictive responsiveness to a,-adrenergic stimulation has recently been reported, 6 but in light of the above findings, we suggest that this is related to structural vessel alterations (see below) rather than to a specific alteration in a^-adrenergic responsiveness.…”

Antidiuretic and antinatriuretic response to high salt load in normotensive Wistar-Kyoto rats: Role of alpha-1A-adrenoreceptors

“…The renal artery infusion of phenylephrine in the second phase did not bring any major change in the MAP and RAP, but was sufficient to cause an antinatriuresis and antidiuresis, further strengthening the fact that, α 1 -adrenoceptor either by renal nerve stimulation or exogenously administered α 1 -adrenoceptor agonist, leads to antidiuresis and antinatriuresis. 36,37 In the third phase of the experiment, phenylephrine infusion was undertaken under the presence of specific α 1A -adrenoceptors antag- This particular finding specifies that the α 1A -adrenoceptors plays a major role in the observed antidiuresis and antinatriuresis in WKYNNa when compared to WKYHNa.…”