Influence of Adrenergic Blocking Drugs on Central Angiotensin Effects

Severs, W B; Summy-Long, Joan Y.; Daniels-Severs, A; Connor, John D.

doi:10.1159/000136192

Cited by 50 publications

(17 citation statements)

References 10 publications

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“…The ANG-SPON rats were allowed to drink 5 ml water after return to their cages. This approximates the mean drinking response to angiotensin [14,15] and matches the degree of hydration produced in the other test procedures. How ever, a 5-10-min differential in the time of water loading is introduced between the groups.…”

Section: Methodssupporting

confidence: 71%

“…In addition, angiotensin is a potent dipsinogenic substance [14,15]. These effects, if uncompensated, would eventually lead to hypotonicity of body fluid compartments.…”

Section: Discussionmentioning

confidence: 99%

“…When in contact with appropriate structures of the brain, angiotensin causes marked drinking behavior [14,15]. In addi tion, intraventricular (IVT) injection of the peptide produces a pressor response in rats, part of which is mediated by the release of a humoral material [14].…”

Section: Introductionmentioning

confidence: 99%

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Effects of Centrally Administered Angiotensin II on Salt and Water Excretion

Severs¹,

Daniels-Severs²,

Summy-Long³

et al. 1971

Pharmacology

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Adult male rats (n = 34) acclimated to metabolism cages received 5 µl artificial cerebrospinal fluid (CSF) with or without 0.5 µg angiotensin intraventricularly (IVT). Urinary volume, Potassium excretion sodium and potassium were followed for 3 h. With a suitable recovery time between experiments every rat was randomly exposed to each of 3 test procedures and thus participated in both control and experimental conditions. The procedures consisted of (1) administration of CSF IVT after gentle bladder massage and of 5 ml water by stomach tube – CSF-PO group; (2) same, except angiotensin was injected IVT – ANG-PO group; (3) same as the ANG-PO group except the stomach tube insertion was a sham procedure; the rats were allowed to drink 5 ml water in response to angiotensin – ANG-SPON group. The angiotensin-induced drinking of 5 ml water took 5–10 min. Except for the 5 ml allowed ANG-SPON rats, water was withheld from all groups during the 3-hour experimental period, and spontaneously voided urine was collected every 15 min. The results of these experiments showed that centrally administered angiotensin produced significant (p < 0.05) antidiuresis for 90 min. During this interval animals receiving angiotensin concentrated sodium and potassium in the urine (p < 0.01) and excreted equal or more absolute sodium and potassium than controls. During the interval from about 90–135 min, when the antidiuresis was over, angiotensin-treated rats excreted more urine of slightly greater sodium and potassium concentration than controls. Hence, angiotensin-treated rats had a significant deficit (p < 0.05) in absolute sodium and potassium when their urine volume became equal to control. During the 3rd h, all groups excreted similar volumes of urine. Both angiotensin groups recovered from the observed sodium loss during this time, but they still had a Significant deficit (p < 0.05) in absolute potassium at the termination of the experiment. These central effects of angiotensin (drinking, antidiuresis, sodium and potassium loss) suggest that the peptide may cause the central nervous system to perceive a state of hyperosmolality. The response of water ingestion and conservation with simultaneous sodium and potassium loss would then be expected homeostatic mechanisms. Possibly these effects may operate in the pathogenesis of certain clinical disorders of hypoosmolality, such as the syndrome of inappropriate ADH release.

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Section: Methodssupporting

confidence: 71%

“…In addition, angiotensin is a potent dipsinogenic substance [14,15]. These effects, if uncompensated, would eventually lead to hypotonicity of body fluid compartments.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Effects of Centrally Administered Angiotensin II on Salt and Water Excretion

Severs¹,

Daniels-Severs²,

Summy-Long³

et al. 1971

Pharmacology

Self Cite

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show abstract

“…However, the cardiovascular response to circulating vasopressin is enhanced (6). This results in a total pressor response after sympathetic blockade which is not different from the normal response (6,11). Of primary importance to this study, however, is the fact that the pressor response associated with drinking was abolished, indicating that this particular component is of sympathetic origin.…”

mentioning

confidence: 84%

A Pressor Response Associated with Drinking in Rats

Hoffman

Phillips

Wilson

et al. 1977

Experimental Biology and Medicine

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“…Adrenergic neurotransmitters from several hypothalamic areas may participate in the effect of ANGII regulating hydromineral fluid intake and renal electrolyte excretion in a process that involves α 1 -and α 2 -adrenoceptors (3)(4)(5). Central injection of an α-adrenergic antagonist suppresses water intake induced by intracerebroventricular (icv) ANGII (6,7). Several areas of the limbic system participate in the regulation of sodium, potassium and water excretion (8).…”

Section: Introductionmentioning

confidence: 99%

Adrenoceptors of the medial septal area modulate water intake and renal excretory function induced by central administration of angiotensin II

Saad

Guarda

Camargo

et al. 2002

Braz J Med Biol Res

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We investigated the role of α-adrenergic antagonists and clonidine injected into the medial septal area (MSA) on water intake and the decrease in Na + , K + and urine elicited by ANGII injection into the third ventricle (3rdV). Male Holtzman rats with stainless steel cannulas implanted into the 3rdV and MSA were used. ANGII (12 nmol/µl) increased water intake (12.5 ± 1.7 ml/120 min). Clonidine (20 nmol/ µl) injected into the MSA reduced the ANGII-induced water intake (2.9 ± 0.5 ml/120 min). Pretreatment with 80 nmol/µl yohimbine or prazosin into the MSA also reduced the ANGII-induced water intake (3.0 ± 0.4 and 3.1 ± 0.2 ml/120 min, respectively). Yohimbine + prazosin + clonidine injected into the MSA abolished the ANGIIinduced water intake (0.2 ± 0.1 and 0.2 ± 0.1 ml/120 min, respectively). ANGII reduced Na + (23 ± 7 µEq/120 min), K + (27 ± 3 µEq/120 min) and urine volume (4.3 ± 0.9 ml/120 min). Clonidine increased the parameters above. Clonidine injected into the MSA abolished the inhibitory effect of ANGII on urinary sodium. Yohimbine injected into the MSA also abolished the inhibitory effects of ANGII. Yohimbine + clonidine attenuated the inhibitory effects of ANGII. Prazosin injected into the MSA did not cause changes in ANGII responses. Prazosin + clonidine attenuated the inhibitory effects of ANGII. The results showed that MSA injections of α 1 -and α 2 -antagonists decreased ANGII-induced water intake, and abolished the Na + , K + and urine decrease induced by ANGII into the 3rdV. These findings suggest the involvement of septal α 1 -and α 2 -adrenergic receptors in water intake and electrolyte and urine excretion induced by central ANGII. Correspondence

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Influence of Adrenergic Blocking Drugs on Central Angiotensin Effects

Cited by 50 publications

References 10 publications

Effects of Centrally Administered Angiotensin II on Salt and Water Excretion

Effects of Centrally Administered Angiotensin II on Salt and Water Excretion

A Pressor Response Associated with Drinking in Rats

Adrenoceptors of the medial septal area modulate water intake and renal excretory function induced by central administration of angiotensin II

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