Key result
In conscious stroke-prone spontaneously hypertensive rats, pressor responses to noradrenaline and hypotensive responses to acetylcholine were enhanced, while reflex bradycardia and hypotensive responses to adenosine were attenuated compared to normotensive rats.
Why the study?
Does intravenous administration of endogenous vasoactive agents alter blood pressure and heart rate differently in conscious stroke-prone spontaneously hypertensive rats compared to normotensive rats?
Does intravenous administration of endogenous vasoactive agents alter blood pressure and heart rate differently in conscious stroke-prone spontaneously hypertensive rats compared to normotensive rats?
Answers are grounded in this paper and cite their sources.
In conscious stroke-prone spontaneously hypertensive rats, enhanced pressor responses to noradrenaline and attenuated hypotensive responses to adenosine may contribute to the development and maintenance of hypertension.
The effects of the endogenous pressor agents noradrenaline (NA), and angiotensin II (Ang II), and of the hypotensive agents acetylcholine (ACh) and adenosine (ADS), on blood pressure and heart rate in conscious and unrestrained stroke-prone spontaneously hypertensive rats (SHR-SP) and normotensive Wistar Kyoto rats (WKY) of different ages (4-9 weeks old) were investigated. Pressor responses to NA were enhanced in 7- and 9- week-old SHR-SP compared with those in WKY, but pressor responses to Ang II in SHR-SP were not different from those in WKY at all ages. The bradycardias following pressor responses to NA and Ang II were markedly attenuated in SHR-SP, especially older ones. Hypotensive responses to ACH were enhanced in SHR-SP, particularly at 9 weeks of age. However, hypotensive responses to ADS were attenuated in SHR-SP, especially at 7 weeks of age. Transient fall of heart rate due to ADS was also attenuated in 7- and 9- week-old SHR-SP. These alterations of hemodynamic or cardiovascular responses in SHR-SP became more evident in the established stages of hypertension. These results suggest intimate relationships of the enhanced pressor responses to NA, attenuated bradycardias following pressor effects with NA or Ang II, and the attenuated hypotensive responses to ADS with the development or the maintenance of hypertension in SHR-SP.
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Hara et al. (1993) studied Hypertension. Endogenous pressor and hypotensive agents (noradrenaline, angiotensin II, acetylcholine, adenosine) vs. Normotensive Wistar Kyoto rats (WKY) was evaluated on Blood pressure and heart rate responses. In conscious stroke-prone spontaneously hypertensive rats, pressor responses to noradrenaline and hypotensive responses to acetylcholine were enhanced, while reflex bradycardia and hypotensive responses to adenosine were attenuated compared to normotensive rats.
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