Different effects on rat arterial pressure and heart rate when losartan is injected into the third or fourth ventricle

Carciovascular responses to central losartan (LOS), a non-peptide angiotensin II (ANG II) receptor antagonist, were investigated by comparing the effects of LOS injection into the 3rd and 4th cerebral ventricles (3rdV, 4thV) on mean arterial pressure (MAP) and heart rate (HR). Adult male Holtzman rats were used (N = 6 animals per group). Average basal MAP and HR were 114 + or - 3 mmHg and 343 + or - 9 bpm (N = 23), respectively. LOS (50, 100 or 200 nmol/2 µl) injected into the 3rdV induced pressor (peak of 25 + or - 3 mmHg) and tachycardic (peak of 60 + or - 25 bpm) responses. LOS injected into the 4thV had no effect on MAP, but it induced bradycardia (peak of -35 + or - 15 bpm). KCl (200 nmol/2 µl) injected into the 3rdV or into the 4thV had no effect on either MAP or HR compared to 0.9 percent saline injection. The results indicate that LOS injected into the third ventricle acts on forebrain structures to induce its pressor and tachycardic effects and that bradycardia, likely dependent on hindbrain structures, is obtained when LOS is injected into the fourth ventricle

Lesions of the lateral hypothalamus impair the pressor response to clonidine injected into the medial septal area of conscious rats

The central injection of clonidine (an alpha2-adrenoceptor agonist) in conscious normotensive rats produces hypertensive responses and breadycardia. The present study performed was performed to investigate the effect of electrolytic lesions of the lateral hypothalamus (LH) on the pressor and bradycardiac responses induced by clonidine injected into the medial septal area (MSA) in conscious and unrestrained rats. Male Holtzman rats weighing 250-300 g were used. Mean arterial pressure and heart rate were recorded in sham- or bilateral LH-lesioned rats with a cerebral stainless steel cannula implanted into the MSA. The injection of clonidine (40 nmol/ul) into the MSDA of sham rats (N=8) produced a pressor response (36 ñ 7 mmHg, P<0.05) and bradycardia (-70 ñ 13 bpmm, P<0.05) compared to saline. Fourteen days after LH-lesion (N=9) the pressor response was reduced (9 ñ 10 mmHg, P<0.05) but no change was observed in the bradycardia (-107 ñ 24 bpm). These results show that LH is an important area involved in the pressor response to clonidine injected into the MSA of rats

The effect of phentolamine on the pressor reponse to centrallly administered clonidine in rats

In the present study we investigae the effect of the previous injection of phentolamine (anonspecific alfa-adrenergic antagonist) into the lateral hypothalamus (LH) and lateral ventricle (LV) on the pressor and bradycardic responses produced by the injection of clonidine (an alfa-2 adrenergic agonist) into these same areas of conscious rats. The injections of clonidine into the LH produced pressor (39 ñ 5 and 38 ñ 3 mmHg, respectively) and bradycardic responses (-65 ñ 16 and -94 ñ 13 bpm, respectively). Previous injections of phentalamine into the LH or LV reduced the pressor response to clonidine injected into the same areas (DeltaMAP = 13 ñ 6 mmHg for LH and 1 ñ 3 mmHg for LV). No reduction was observed when clonidine was injected into the LV after the injection of phentalamine into the LH. No changes in bradycardic responses were observed after treatment with phentolamine. The present results show the participation of alfa-adrenergic receptors in the pressor response to centrally administered clonidine but not in the bradycardic reponse. The data also suggest that the pressor effect by the injection of clonidine into the LH is due to the activation of alfa-adrenergic receptors located specifically in this area. The pressor response after injection of clonidine into the LV and of phentolamine into the LH is due to the action of clonidine on other cerebral areas

Effect of dehydration on the increase of arterial pressure and renal electrolyte excretion produced by central cholinergic stimulation in rats

Natriuresis, kaliuresis, diuresis, arterial pressure and heart rate were studied in rats following dehydration and cholinergic stimulation of the medial septal area (MSA). The increase in renal NA+ and K+ excretion produced by the injection of carbachol (2nmol) into the MSA in normal hydrated rats was abolished in 48-h water-deprived rats. Urinary volume was also reduced. Cholinergic stimulation of the MSA produced a smaller mincrease in arterial pressure in 48-h-deprived rats compared to normal hydrated animals. No change was observed in heart rate. These reults show that hydration state is essential for the central cholinergic control of electrolyte excretion and increase in arterial pressure

Interaction between cholinergic and opiate receptors of the lateral hypothalamus in the control of renal excretion in rats

The present study was carried out to investigate the participation and interaction between cholinergic and opiate receptors of the lateral hypothalamus (LH) in the regulation of Na+, K+ and water excretion. Malew Holtzman rats were implanted with chronic cerebral cannulas into the LH. Urine was collected over a period of 2h after injection of carbachol, FK-33824 + carbachol or naloxone + carbachol into the LH. Carbachol (8nmol) reduced urinary volume and increased Na + excretion. Previous injection of FK-333824(100ng) into the LH increased the antidiuretic effect of carbachol, but blocked the increase in Na+ excretion and decreased K+ excretion. Naloxone. Naloxone (10microng) produced no changes in the effect of carbacho9l on renal excretion. These data show an inhibitory effect of opiate receptors on the changes in urinary Na+ and K+ excretion that are induced by chronergic stimulation of the LH in rats, and a potentiating effect on antidiuresis

Pressor responses of clonidins injected into some prosencephalic areas of conscious rats

The objective of this investigation was to study the effect of clonidine injection into some prosencephalic areas of unanesthetized rats on mean arterial pressure (MAP) and heart rate (HR). Injection of 40 nmol clonidine in 1.0 gama 150 mM NaCl into rhe medial septal area, lateral hypothalamus, lateral preoptic area and lateral ventricle caused the same increase in MAP, 38 ñ 3 to 41 ñ 5 mmHg, and decrease in HR, -65 ñ 10 to -94 ñ 13 bpm (mean ñ SEM, N = 9 to 11 animnals). These results show that clonidine can act on several prosencephalic areas to induce a pressor response in the conscious rat