Presynaptic alpha- and beta-adrenoceptor stimulation and norepinephrine release in the spontaneously hypertensive rat.

Ekas, Robert D.; Steenberg, Marie L.; Woods, Matthew; Lokhandwala, Mustafa F.

doi:10.1161/01.hyp.5.2.198

Cited by 61 publications

(12 citation statements)

References 25 publications

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“…Our present results are in agreement with those re ported by Ekas et al [5] who also found a similar presynaptic (3-receptor function in NR and SHR. For the mes enteric vascular bed of the SHR, however, it was shown that the (32-adrenoceptor-mediated facilitatory modula tion of vascular neurotransmission was enhanced com pared with that of NR [4].…”

Section: Discussionsupporting

confidence: 94%

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Study of Prejunctional Beta-Adrenoceptors in Kidneys of Normotensive and Hypertensive Rats Using the New Beta-Adrenoceptor Blocking Drug Tertatolol

Verbeuren¹,

Herman²

1986

Am J Nephrol

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The prejunctional β-adrenoceptors present in the isolated perfused kidney of normotensive rats (NR) and spontaneously hypertensive rats (SHR) were compared and the effects of tertatolol on these receptors were investigated. Kidneys of NR (Wistar + Wistar-Kyoto [WKY]) and SHR, were continuously perfused with Tyrode solution at constant flow and the changes in perfusion pressure were monitored. The constrictor responses to norepinephrine (2–8 × 10^-10 moles) were slightly but significantly decreased by isoproterenol (2 × 10^-7M) to a similar degree in NR and SHR. Tertatolol (3 X 10^-7M) did not alter the constriction caused by norepinephrine, but abolished the dilator response to isoproterenol. Electrical stimulation of renal nerves (8 Hz) evoked constrictions in both NR and SHR; these constrictor responses were augmented in the presence of isoproterenol (2 × 10^-7M) to a similar extent in NR and SHR. In kidneys of NR and SHR, previously incubated with ³H norepinephrine, renal nerve electrical stimulation (6 Hz) evoked an overflow of the ³H transmitter. This overflow was enhanced by isoproterenol (2 × 10^-6M) to a similar degree in NR and SHR. Both the augmented constrictor response and the augmented overflow of ³H norepinephrine caused by electrical stimulation in the presence of isoproterenol, were inhibited by tertatolol (3 X 10^-7M). Our results show that the β-receptor agonist isoproterenol evokes comparable effects at prejunctional β-adrenoceptors in kidneys of NR and SHR; they also show that tertatolol is an inhibitor of pre- and postjunctional β-adrenoceptors in the renal circulation of the rat.

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Section: Discussionsupporting

confidence: 94%

“…Whether these prejunctional p-receptors are modified in SHR is debatable; an enhanced presynaptic P-adrenoceptor-mediated modulation of adrenergic neurotrans mission has been reported for the perfused mesenteric bed of SHR [4], whereas an unchanged presynaptic Padrenoceptor function was reported for the perfused kid ney of SHR [5].…”

Section: Introductionmentioning

confidence: 99%

Study of Prejunctional Beta-Adrenoceptors in Kidneys of Normotensive and Hypertensive Rats Using the New Beta-Adrenoceptor Blocking Drug Tertatolol

Verbeuren¹,

Herman²

1986

Am J Nephrol

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“…Yohimbine adminis tration to SHR produces a significant reduc tion in renal NE content down to WKY lev els [38]. Other studies also confirm an al tered renal responsiveness to a 2-adrcncrgic drugs in the SHR when compared to the WKY [39], Thus, the changes in Ra2AR number in the SHR correlates with func tional abnormalities.…”

Section: Discussionmentioning

confidence: 85%

Renal Catecholamines and α<sub>2</sub>-Adrenergic Receptors in Salt-Related and Genetic Hypertension

Dawson¹,

Oparil²

1987

Pharmacology

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Increased dietary salt intake alters renal function which often leads to deleterious cardiovascular consequences. Studies were carried out to characterize the effects of high-salt diets on renal catecholamines and α₂-adrenergic receptors. These parameters were evaluated in both genetic and acquired forms of hypertension and also in normotensive rats on high-salt diets. Renal catecholamine content was determined by high-performance liquid chromatography with electrochemical detection. Renal α₂-adrenergic receptor-binding studies were performed on whole kidney homogenates using ³H-p-aminoclonidine to label both high- (0.5 nM) and low-affinity (5.0 nM) renal α₂-adrenergic receptors. Increased salt intake elevated blood pressure, decreased renal norepinephrine stores and resulted in renal α₂-adrenergic receptor up-regulation in deoxycorticosterone acetate salt hypertensive rats, Dahl-S rats and COX-SHR. The decreased renal stores of norepinephrine (NE) appeared to reflect increased renal NE utilization. In contrast, SHR (Charles River) had elevated NE stores and α₂-adrenergic receptors while on normal salt diets. Short-term (10–14 days) exposure to high-salt diets had modest effects in normotensive rats or COX-SHR, although it was sufficient to increase low affinity renal α1-adrenergic receptor number. Renal dopamine metabolism was also altered by high-salt diets. These studies demonstrated a relationship between renal NE content and renal α₂-adrenergic receptors. The implications of this relationship and other salt-related changes in renal catecholamine metabolism were discussed as they pertained to hypertension and renal function.

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“…5 -8 In light of the influence of the sympathetic nervous system on sodium and water reabsorption and renovascular tone, the potential importance of the renal nerve in the pathogenesis of experimental hypertension is well recognized. 9 - 10 Particularly compelling is evidence that efferent renal nerve activity is elevated andjunctional norepinephrine release is enhanced 11 …”

mentioning

confidence: 99%

Renal alpha 1-adrenergic receptor response coupling in spontaneously hypertensive rats.

1988

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T HE renal sympathetic nerve plays an important role in renal tubular electrolyte reabsorption and renovascular tone.'-2 Low frequency stimulation of the rat renal nerve causes an a,-adrenergic receptor-mediated increase in tubular sodium and water reabsorption.3 -3 Higher frequency renal nerve stimulation results in renovasoconstriction mediated by a,-adrenergic receptors. 5 -8 In light of the influence of the sympathetic nervous system on sodium and water reabsorption and renovascular tone, the potential importance of the renal nerve in the pathogenesis of experimental hypertension is well recognized.9 -10 Particularly compelling is evidence that efferent renal nerve activity is elevated andjunctional norepinephrine release is enhanced Received February 6, 1987; accepted March 29, 1988. in spontaneously hypertensive rats (SHR) when compared with Wistar-Kyoto rats (WKY) 13 and that renal denervation delays the onset of genetic hypertension. -16 Very recent evidence suggests that neuronal reflexes are impaired in SHR kidneys.17 Since a,-adrenergic receptors mediate important functions of the renal nerve, we hypothesize that this adrenergic receptor subtype plays an integral role in the pathogenesis of hypertension in SHR. Interestingly, it was recently reported 18 that renal membrane a,-adrenergic receptor density is increased in SHR compared with WKY.These findings suggest that a,-adrenergic receptor regulation is defective in SHR, since the receptors fail to down-regulate (and, in fact, are increased in density) under conditions of increased sympathetic nerve activity (and hence, increased junctional norepinephrine concentration or turnover, or both). It has thus been proposed 18 that this defect is responsible for enhanced sodium and water reabsorption and increased renovascular tone in SHR.

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Presynaptic alpha- and beta-adrenoceptor stimulation and norepinephrine release in the spontaneously hypertensive rat.

Cited by 61 publications

References 25 publications

Study of Prejunctional Beta-Adrenoceptors in Kidneys of Normotensive and Hypertensive Rats Using the New Beta-Adrenoceptor Blocking Drug Tertatolol

Study of Prejunctional Beta-Adrenoceptors in Kidneys of Normotensive and Hypertensive Rats Using the New Beta-Adrenoceptor Blocking Drug Tertatolol

Renal Catecholamines and α<sub>2</sub>-Adrenergic Receptors in Salt-Related and Genetic Hypertension

Renal alpha 1-adrenergic receptor response coupling in spontaneously hypertensive rats.

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Presynaptic alpha- and beta-adrenoceptor stimulation and norepinephrine release in the spontaneously hypertensive rat.

Cited by 61 publications

References 25 publications

Study of Prejunctional Beta-Adrenoceptors in Kidneys of Normotensive and Hypertensive Rats Using the New Beta-Adrenoceptor Blocking Drug Tertatolol

Study of Prejunctional Beta-Adrenoceptors in Kidneys of Normotensive and Hypertensive Rats Using the New Beta-Adrenoceptor Blocking Drug Tertatolol

Renal Catecholamines and &alpha;<sub>2</sub>-Adrenergic Receptors in Salt-Related and Genetic Hypertension

Renal alpha 1-adrenergic receptor response coupling in spontaneously hypertensive rats.

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Renal Catecholamines and α<sub>2</sub>-Adrenergic Receptors in Salt-Related and Genetic Hypertension