hello sir here is the possible explaination and reference of your question
Reflex inhibition of sympathetic activity during volume load in awake normotensive and spontaneously hypertensive rats
S.-E. RICKSTEN and
P. THOREN
Article first published online: 8 DEC 2008
DOI: 10.1111/j.1748-1716.1980.tb06632.x
© 1980 Scandinavian Physiological Society
Issue
Acta Physiologica Scandinavica
Acta Physiologica Scandinavica
Volume 110, Issue 1, pages 77–82, September 1980
Keywords:
Awake rats;
sympathetic nerve recording;
SHR;
WKR;
volume load.
The reflex inhibition of the sympathetic activity in the splanchnic nerves was recorded upon volume expansion with blood in awake spontaneously hypertensive rats (SHR) and in normotensive Wistar-Kyoto rats (WKR) at an age of 16–20 weeks. At 10% blood volume expansion SHR showed a significantly greater nerve inhibition (43 %) in comparison with WKR (33 %). This augmented reflex response was not caused by the arterial baroreceptors, because the sensitivity of the arterial baroreceptor reflex arch, if anything, tended to be lower in SHR and the increase in arterial blood pressure upon volume load was also lower in SHR. It is suggested that the reason for this increased reflex inhibition in SHR is an augmented low pressure receptor response. The mechanism behind this is discussed. The most likely explanation is a decreased distensibility of the venous system, the systemic andlor the pulmonary veins.
Non hypotensive hemorrhage simulated by applying low grade (< 20 mmHg) lower body suction pressure is known to increase fore arm vascular resistance in human subjects without changes in heart rate or blood pressure. There is however an increase in circulating nor epinephrine. The reflex has been attributed to deactivation of low pressure cardiovascular receptors. The opposite experiment could be conducted in NORMAL human volunteers by subjecting them to a 5 deg head down tilt or infusion if limited volume of fluid in to the right atrium (theoretically at least) and measuring fore arm vascular resistance. The fore arm vascular resistance should decrease.
The arterial (high pressure) baro receptors are known to be reset in long standing hypertension. But I do not remember references which may have studied low pressure cvs receptors during hypertension. Also is there any evidence that the low pressure receptors are subjected to a continuous high volume load in patients with hypertension? It may be interesting to carry out above mentioned experiments in patients with long standing hypertension.
Best wishes
Mohan B Dikshit>
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