Effects of intracerebroventricular injections of losartan or PD123319 on arterial pressure and heart rate of sodium replete and sodium deplete rats

Luca, Laurival A. De; Barbosa, Silas Pereira; Sugawara, Alexandre Massao; Menani, José Vanderlei

doi:10.1016/0167-0115(96)00055-9

Cited by 14 publications

(22 citation statements)

References 15 publications

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“…When injected into the 4th ventricle, but not into the anterior ventricles, losartan induces bradycardia (1,2) likely related to the modulatory effect hindbrain ANG II receptors have on baroreflex (8)(9)(10)(11)(12). However, better hypertensive effects are obtained with losartan injected into the 3rd than into the 4th cerebral ventricles in the rat (1,2). Contrary to what has been suggested (12), this effect does not depend on potassium associated with losartan (1).…”

Section: Discussioncontrasting

confidence: 41%

“…The AT 1 angiotensin II (ANG II) receptor antagonist losartan induces an increase in arterial pressure when injected into the brain ventricular system (1)(2)(3). Activation of brain ANG II receptors is traditionally associated with an increase in arterial pressure (4,5), but there are also reports of a decrease in arterial pressure induced by exogenous ANG II (for a review, see Ref.…”

Section: Introductionmentioning

confidence: 99%

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Dissociation between the circulating renin-angiotensin system and angiotensin II receptors in central losartan-induced hypertension

Sugawara

Vendramini

Barbosa

et al. 2002

Braz J Med Biol Res

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Losartan, an AT 1 angiotensin II (ANG II) receptor non-peptide antagonist, induces an increase in mean arterial pressure (MAP) when injected intracerebroventricularly (icv) into rats. The present study investigated possible effector mechanisms of the increase in MAP induced by icv losartan in unanesthetized rats. Male Holtzman rats (280-300 g, N = 6/group) with a cannula implanted into the anterior ventral third ventricle received an icv injection of losartan (90 µg/2 µl) that induced a typical peak pressor response within 5 min. In one group of animals, this response to icv losartan was completely reduced from 18 ± 1 to 4 ± 2 mmHg by intravenous (iv) injection of losartan (2.5-10 mg/kg), and in another group, it was partially reduced from 18 ± 3 to 11 ± 2 mmHg by iv prazosin (0.1-1.0 mg/kg), an a 1 -adrenergic antagonist (P<0.05). Captopril (10 mg/kg), a converting enzyme inhibitor, injected iv in a third group inhibited the pressor response to icv losartan from 24 ± 3 to 7 ± 2 mmHg (P<0.05). Propranolol (10 mg/ kg), a ß-adrenoceptor antagonist, injected iv in a fourth group did not alter the pressor response to icv losartan. Plasma renin activity and serum angiotensin-converting enzyme activity were not altered by icv losartan in other animals. The results suggest that the pressor effect of icv losartan depends on angiotensinergic and a 1 -adrenoceptor activation, but not on increased circulating ANG II.

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Section: Discussioncontrasting

confidence: 41%

Section: Introductionmentioning

confidence: 99%

Dissociation between the circulating renin-angiotensin system and angiotensin II receptors in central losartan-induced hypertension

Sugawara

Vendramini

Barbosa

et al. 2002

Braz J Med Biol Res

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“…Note that this hypotension is not the result of an additive effect of the drugs on a preexisting hypotension associated with sodium depletion because MAP of sodium-depleted rats is similar to hydrated controls (10). The unloading of cardiopulmonary receptors by hypotension may facilitate water and sodium intake (24); therefore, it is not possible to exclude some influence of the hypotension facilitating 0.3 M NaCl intake after the combination of YOH and LPS.…”

Section: Sodium Appetite Test and Changes In Map And Hr In Sodium-depmentioning

confidence: 99%

“…We combined the diuretic and natriuretic furosemide with 24-h removal of ambient sodium to deplete the animals of sodium (10,24,(35)(36)(37).…”

Section: Sodium Depletion and Sodium Appetite Testmentioning

confidence: 99%

“…Moreover, recall that a strong motivation also may overcome the inhibitory effect of LPS (7). Therefore, it is important to test if, independent from its antinatriuretic effects, LPS also inhibits sodium appetite, a motivated behavior fully expressed after several hours of sodium depletion (10,24,(35)(36)(37). Such test may be performed by sodium depleting the animals, for example, through the combination of furosemide injection plus 24-h removal of ambient sodium (10, 24, 35-37) before injecting LPS.…”

mentioning

confidence: 99%

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Inhibition of sodium appetite by lipopolysaccharide: involvement of α₂-adrenoceptors

Almeida

David²,

Constancio³

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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Lipopolysaccharide (LPS), an endotoxin from the wall of Escherichia coli, produces a general behavioral inhibition and affects several aspects of fluid-electrolyte balance. LPS inhibits thirst; however, it is not clear if it also inhibits sodium appetite. The present results show that LPS (0.3-2.5 mg/kg body wt) injected intraperitoneally produces a dose-dependent reduction of sodium appetite expressed as 0.3 M NaCl intake induced by sodium depletion (furosemide plus removal of ambient sodium for 24 h). The high doses of LPS (1.2-2.5 mg/kg) also produced transient hypothermia at the beginning of the sodium appetite test; however, no dose produced hyperthermia. LPS also increased the stomach liquid content (an index of gastric emptying) after a load of 0.3 M NaCl given intragastrically by gavage to sodium-depleted rats. The ␣ 2-adrenoceptor antagonist yohimbine (5 mg/kg ip) abolished the effect of LPS on 0.3 M NaCl intake, without changing the effect of LPS on gastric emptying. Injection of RX-821002 (160 nmol), another ␣ 2-adrenoceptor antagonist, in the lateral cerebral ventricle (LV) also reversed the inhibition of sodium appetite produced by LPS. Yohimbine intraperitoneally or RX-821002 in the LV alone had no effect on sodium intake. Although yohimbine plus LPS produced a slight hypotension, RX-821002 plus LPS produced no change in arterial pressure, suggesting that the blockade of the effects of LPS on sodium intake by the ␣ 2-adrenoceptor antagonists is independent from changes in arterial pressure. The results suggest an inhibitory role for LPS in sodium appetite that is mediated by central ␣ 2-adrenoceptors. sodium intake; endotoxin; arterial pressure; RX-821002; fluid balance; sickness behavior LIPOPOLYSACCHARIDE (LPS), an endotoxin derived from the wall of gram-negative bacteria, triggers an array of behavioral and systemic responses, grouped under the name of "sickness behavior" (7).Sickness behavior has been hypothesized to be an adaptive syndrome of behavioral and physiological responses by animals coping with infectious pathogens (7). Reduced activity, feeding, and drinking are some of the behavioral alterations induced by infection. These alterations may help to shift internal energy production to increase body temperature and sustain fever, an important mechanism to combat infection.It is possible that the reduced drinking that occurs in sickness behavior is also associated with a general effect on body-fluid balance because LPS releases hormones that influence such balance (4) and reduces several aspects related to sodium metabolism: sodium transport in the gut (5), natriuresis (1, 31), and a rapidly developing sodium intake induced by the diuretic furosemide combined with a low dose of the converting enzyme inhibitor captopril or Furo/Cap (1).In the previous study (1), LPS injected before Furo/Cap treatment inhibited sodium intake produced within 2 h, but it also reduced sodium excretion, which may affect sodium intake. Thus it is not possible to definitively conclude if the inhibition of sodiu...

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Effects of intracerebroventricular losartan on angiotensin II‐mediated pressor responses and c‐fos expression in near‐term ovine fetus

Shi¹,

Mao²,

Thornton³

et al. 2005

J of Comparative Neurology

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The renin-angiotensin system plays an important role in cardiovascular control. Intracerebroventricular (i.c.v.) angiotensin (ANG) II causes a reliable pressor response in the fetus at 90% gestation. To determine the roles of brain AT1 and AT2 receptors in this response, the effects of the central AT1 and AT2 receptor antagonists losartan and PD123319 were investigated in chronically prepared near-term ovine fetuses. Losartan at 0.5 mg/kg (i.c.v.) abolished central ANG II-induced pressor responses. High-dose losartan (5 mg/kg, i.c.v.) showed a potentiation of the pressor response to i.c.v. ANG II, accompanied by bradycardia. Associated with the pressor responses, c-fos expression in the cardiovascular controlling areas was significantly different between the low and high doses of losartan. These areas included the subfornical organ, median preoptic nucleus, organum vasculosum of the lamina terminalis, and paraventricular nuclei in the forebrain, and the tractus solitarius nuclei, lateral parabrachial nuclei in the hindbrain. Low-dose losartan markedly reduced c-fos in these areas after i.c.v. ANG II, while the high-dose losartan together with ANG II elicited a much stronger FOS-immunoreactivity in these areas than that induced by i.c.v. ANG II alone. This is a novel finding, that c-fos expression in the brain can be both activated and inhibited under the same condition. Central ANG II-induced fetal pressor responses were not altered by PD123319 (0.8 mg/kg). These results indicate that i.c.v. losartan at a high and a low dose has strikingly different effects on central ANG II-induced pressor responses in fetuses at late gestation, and that the AT1 mechanism plays an important role in fetal cardiovascular regulation.

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Effects of intracerebroventricular injections of losartan or PD123319 on arterial pressure and heart rate of sodium replete and sodium deplete rats

Cited by 14 publications

References 15 publications

Dissociation between the circulating renin-angiotensin system and angiotensin II receptors in central losartan-induced hypertension

Dissociation between the circulating renin-angiotensin system and angiotensin II receptors in central losartan-induced hypertension

Inhibition of sodium appetite by lipopolysaccharide: involvement of α₂-adrenoceptors

Effects of intracerebroventricular losartan on angiotensin II‐mediated pressor responses and c‐fos expression in near‐term ovine fetus

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Effects of intracerebroventricular injections of losartan or PD123319 on arterial pressure and heart rate of sodium replete and sodium deplete rats

Cited by 14 publications

References 15 publications

Dissociation between the circulating renin-angiotensin system and angiotensin II receptors in central losartan-induced hypertension

Dissociation between the circulating renin-angiotensin system and angiotensin II receptors in central losartan-induced hypertension

Inhibition of sodium appetite by lipopolysaccharide: involvement of α2-adrenoceptors

Effects of intracerebroventricular losartan on angiotensin II‐mediated pressor responses and c‐fos expression in near‐term ovine fetus

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Inhibition of sodium appetite by lipopolysaccharide: involvement of α₂-adrenoceptors