Neurogenic hypertension and elevated vertebrobasilar arterial resistance: is there a causative link?

There is evidence of sympathetic overdrive in a significant proportion of patients with essential hypertension and an animal model of the condition, the spontaneously hypertensive rat (SHR). The reasons for this remain elusive. However, there is also evidence of narrowing of the arteries supplying the brainstem in the SHR and hypertensive humans. In this review, we discuss the possible role of brainstem hypoperfusion in driving increased sympathetic activity and hypertension.

Strokes and their relationship to hypertension.

PURPOSE OF REVIEW: There is rapidly growing appreciation that stroke morbidity and the risk of an ischaemic stroke becoming haemorrhagic can be influenced by new information about prophylaxis, rapid diagnosis and treatment. RECENT FINDINGS: Strokes are strongly associated with hypertension mainly because hypertension is strongly associated with atheromatous deposits blocking or narrowing brain arteries, predisposing to local clot formation. Atheroma and its ischaemic consequences may damage cerebral arterioles and the brain tissue they supply. Cerebral infarcts are more common than spontaneous cerebral haemorrhages. High blood pressure itself cannot directly rupture cerebral blood vessels because their small size protects them and intracerebral haemorrhage usually follows previous ischaemic vascular damage. It is obvious that lowering blood pressure would reduce the risk and extent of bleeding into the brain once a break in an arteriolar wall has occurred, but it is not clear why lowering blood pressure should protect against cerebral infarction. One might expect that slowing down the rate of cerebral blood flow would give more time for local clots to form. It seems most likely that induced hypotension protects against ischaemic strokes by preventing pressure- or ischaemia-induced arteriolar spasm and by advantageous vasodilation of some of the more ischaemic territories. Added protection can be provided by coenzyme-A reductase inhibitors (statins), but probably not by antioxidants. SUMMARY: Lowering blood pressure strongly protects against ischaemic and haemorrhagic stroke. Recent work shows that more accurate and faster diagnosis of stroke pathology is urgently needed, so that appropriate treatment (e.g. with tissue plasminogen activators) can be started before local bleeding has occurred.