Mean Arterial Pressure In Animals Research Articles

Switching control of sympathetic activity from forebrain to hindbrain in chronic dehydration

We investigated the mechanisms responsible for increased blood pressure and sympathetic nerve activity (SNA) caused by 2-3 days dehydration (DH) both in vivo and in situ preparations. In euhydrated (EH) rats, systemic application of the AT(1) receptor antagonist Losartan and subsequent pre-collicular transection (to remove the hypothalamus) significantly reduced thoracic (t)SNA. In contrast, in DH rats, Losartan, followed by pre-collicular and pontine transections, failed to reduce tSNA, whereas transection at the medulla-spinal cord junction massively reduced tSNA. In DH but not EH rats, selective inhibition of the commissural nucleus tractus solitarii (cNTS) significantly reduced tSNA. Comparable data were obtained in both in situ and in vivo (anaesthetized/conscious) rats and suggest that following chronic dehydration, the control of tSNA transfers from supra-brainstem structures (e.g. hypothalamus) to the medulla oblongata, particularly the cNTS. As microarray analysis revealed up-regulation of AP1 transcription factor JunD in the dehydrated cNTS, we tested the hypothesis that AP1 transcription factor activity is responsible for dehydration-induced functional plasticity. When AP1 activity was blocked in the cNTS using a viral vector expressing a dominant negative FosB, cNTS inactivation was ineffective. However, tSNA was decreased after pre-collicular transection, a response similar to that seen in EH rats. Thus, the dehydration-induced switch in control of tSNA from hypothalamus to cNTS seems to be mediated via activation of AP1 transcription factors in the cNTS. If AP1 activity is blocked in the cNTS during dehydration, sympathetic activity control reverts back to forebrain regions. This unique reciprocating neural structure-switching plasticity between brain centres emphasizes the multiple mechanisms available for the adaptive response to dehydration.

Cardiovascular effects of elgodipine and nifedipine compared in anaesthetized rats

The cardiovascular effects of elgodipine were studied and compared with those of nifedipine in the presence or absence of ganglion blockade. A bolus of elgodipine (5–25 μg/kg) or nifedipine (60–120 μg/kg) was given and sequential cardiovascular effects in rats were recorded. Both dihydropyridines induced a dose-dependent decrease in mean arterial pressure but, whereas nifedipine induced reflex tachycardia, elgodipine induced a dose-dependent bradycardia. Both substances induced decreases in left ventricular d P/d t max without significant changes in central venous pressure. Good linear correlation was observed between the elgodipine-induced decrease in mean arterial pressure and those of heart rate and left ventricular d P/d t max. The profile of the decrease in mean arterial pressure in animals pretreated with hexametonium chloride (20 mg/kg) was the same but the nifedipine-induced tachycardia was abolished without changes in elgodipine-induced bradycardia. These characteristics of elgodipine makes this dihydropyridine a potentially beneficial therapeutic agent in the case of severe hypertension accompanied by obstructive coronopathy.