Role of the Parasympathetic Nervous System and Interaction with the Sympathetic Nervous System in the Early Phase of Hypertension

Abstract

The role of the peripheral parasympathetic nervous system in the development of hypertension was investigated in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. Animals were 5-7 weeks old, anesthetized, and in the open-chest condition. The decrement in heart rate evoked by parasympathetic nerve stimulation (62 +/- 8 beats/min) in SHR was greater (p < 0.01) than that in WKY rats (23 +/- 4 beats/min). Furthermore, the decrease in heart rate (73 +/- 9 beats/min) in response to combined stimulation of sympathetic and parasympathetic nerves in SHR was greater (p < 0.05) than that in response to vagal stimulation alone. The extent of the interaction of sympathetic and parasympathetic nerves was calculated as the difference between the decrease in heart rate during combined stimulation and that during vagal nerve stimulation alone. The extent of the interaction in SHR (-11 +/- 5) was not significantly different from that in WKY rats (-8 +/- 3 beats/min). Therefore, the influence of the peripheral parasympathetic nervous system in the early phase of hypertension may be greater than that in the normotensive state. Interaction between the two branches of the autonomic nervous system may occur as accentuated antagonism originating in the early phase of hypertension. The interaction during the early phase of hypertension may not be different in extent from that of the normotensive state.

Central vagal activation by alpha2‐adrenergic stimulation is impaired in spontaneously hypertensive rats

“…3), suggesting that peripheral vagal con-trol of ACh release was preserved in SHR. Although ex vivo HR response to vagal nerve stimulation is attenuated in SHR compared to WKY in an isolated atrial/right vagus preparation (Heaton et al 2007), in vivo HR response to vagal nerve stimulation is not different between WKY and SHR or is enhanced in SHR than in WKY depending on the age investigated (Ferrari et al 1992, Minami & Head 2000, Masuda 2000. In the present study, HR response to vagal nerve stimulation tended to be enhanced in SHR, consistent with previous in vivo investigations.…”

Gut–Brain Axis in Regulation of Blood Pressure

“…Overactive SNS is present in all the aforementioned conditions, suggesting a significant role in the pathophysiology of treatment resistance. In addition to chronically elevated SNS activity (Tsioufis et al, 2011 ) accompanied by norepinephrine (NE) spillover (Tsioufis et al, 2011 ), dampened parasympathetic activity (Masuda, 2000 ) is also among several common characteristics of resistant HTN, indicating a neurogenic component that contributes to the initiation, maintenance and progression of HTN. Increasing evidence also suggests that, coupled to autonomic dysfunction, treatment-resistant HTN is accompanied by a chronic low-grade inflammatory profile that facilitates end-organ damage and perpetuates the hypertensive state (Grassi et al, 2011 ), suggesting a close link between SNS and the IS.…”

Sports Activities and Activity of Autonomic Nervous System in Cardiac Rhythm

“…따라서 심장 활동이 저하되면, 심장은 전기 생리학적으로 불안정한 상태가 된다 (Billman, 2009). 만성심부전, 당뇨병 및 고 혈압 등의 환자는 심장부교감신경계 활동의 저하가 나 타나는 경우도 있으며, 심근경색환자에게서 심장부교감 신경 활동에 저하가 생길 경우에는 그 예후가 나빠지 는 것으로 보고되어 있다 (Masuda, 2000;Schauerte et al, 2001). 또한 노화에 있어서도 심장부교감신경계 활 동이 저하 된다 (Chow et al, 2001).…”

“…심박변동의 주파수 강도 개의 심박변동의 주파수 강도(A), 부교감신경 차단 및 부교감신경과 교감신경 베타 아드레날린 차단하에서의 심박변동의 주파수 강도(B) (Akserlod et al, 1981). (Wheeler & Watkins, 1973), 고혈압 (Guzzetti et al, 1991;Masuda, 2000), 및 만성심부전 (Machado et al, 2000;Smith et al, 1989)등의 환자에게 심장교감 신경계 활동의 저하가 확인되어 있으며, 심근경색환자 에게 심장교감신경계 활동의 저하가 생길 경우에는 생 명예후가 나쁜 것으로 보고되었다 (Bigger et al, 1992). (Herbert & Bolter, 2002;Perini et al, 1989).…”