Baroreceptor-heart Reflex Research Articles

Effects of central angiotensin II and angiotensin III on baroreflex regulation

In the present study the cardiovascular effects of intracerebroventricularly (i.c.v.) applied angiotensin II (AN II) and angiotensin III (AN III) were analysed in conscious Wistar rats. The baroreceptor heart reflex (BHR) was elicited by intravenous bolus injection of both phenylephrine (1 μg) and sodium nitroprusside (5 μg) before and after i.c.v. administration (1.5 and 15 min) of the peptides. Administration of 20 ng and 200 ng AN II produced a short increase in inter-beat interval (IBI) and a long-lasting increase in mean blood pressure (MBP), inclusive of a drinking response. Only after the high dose of 200 ng AN II we found a continuous impairment in the BHR for reflex bradycardia. Inversely, the small doses of both 100 pg AN II and 100 pg AN III were without effects on IBI and MBP; they induced an enhancement in BHR for the reflex bradycardia and after 100 pg AN II it was also found for the reflex tachycardia. Pretreatment with 20 nmol amastatin (AM), a specified aminopeptidase A inhibitor, followed by 100 pg An II suppressed the enhancement in BHR. AM alone was without effects in this respect. These findings suggest that: 1) the influence of central angiotensin on the BHR could be dose-dependent in the opposite way and 2) AN III seems to be the active form and involved in the central blood pressure regulatory mechanism.

Effects of central Substance P on baroreflex regulation

The effects of intracerebroventricularly (i.c.v.) administered Substance P (100 pg, 1 μg, 10μg) on mean blood pressure (MBP), inter-beat interval (IBI) and the baroreceptor heart reflex (BHR) were studied in conscious Wistar rats. The BHR was induced by intravenous injection of both phenylephrine (1 μg) and sodium nitroprusside (5 μg) before and after SP administration (3 and 15 min). The dose of 100 pg SP was without effect on the resting values of both MBP and IBI but enhanced the BHR sensitivity by about + 0.5 ms/mm Hg in the phenylephrine test 3 min after i.c.v. SP. 1 μg and 10 μg SP caused a long-lasting dose dependent increase in MBP and changed the IBI. In contrast to the results obtained with 100 pg, the BHR sensitivity was impaired-1μg SP:−0.2 ms/mm Hg (phenylephrine) and −0.45 ms/mm Hg (nitroprusside), 10 μg SP: −0.35 ms/mm Hg (phenylephrine). These changes in BHR sensitivity were only recognised 3 min, but not 15 min, after i.c.v. treatment even though changes in the resting values of MBP and IBI were still present at 15 min. These data suggest that SP through the cerebrospinal fluid may participate in central cardiovascular control and, moreover, it may influence the baroreflex regulation.

Cardiovascular Responses to Centrally Applied Sodium Chloride Solution

In conscious and anaesthetized rats the baroreceptor heart reflex (BHR) was checked before and after i.c.v. application of isotonic or hypertonic (0.6 M; 1.0 M) NaCl solution, artificial cerebrospinal fluid (aCSF) and 1.0 M mannitol solution. The BHR was tested by evaluating the alteration of the inter-beat interval (IBI) in response to an artificial BP rise or drop which had been evoked by i.v. bolus injection of either phenylephrine or sodium nitroprusside. The slope of the correlation function was taken to index the reflex sensitivity. In anaesthetized rats the mean sensitivity of the BHR was 0.6 ms/mm Hg (phenylephrine). l.c.v. administration of isotonic NaCl solution did not change BP, IBI or the BHR sensitivity, whilst i.c.v. infusion of hypertonic NaCl solution increased BP and shortened IBI. The BHR sensitivity was impaired only when 1.0 M NaCl solution was i.c.v. infused by 0.23 ms/mm Hg. In conscious rats the mean sensitivity of the BHR was 1.14 ms/mm Hg (phenylephrine) and 1.35 ms/mm Hg (sodium nitroprusside). In the conscious rats i.c.v. bolus injection of hypertonic NaCl solution increased BP as in anaesthetized rats, however, the IBI was prolonged, whilst 1.0 M mannitol solution and aCSF were without any influence on BP, IBI and BHR. l.c.v. administration of hypertonic NaCl solution reduced the BHR sensitivity by approximately 0.6 ms/mm Hg.