NDLI: Amplified respiratory–sympathetic coupling in the spontaneously hypertensive rat: does it contribute to hypertension?

Content Provider	PubMed Central
Author	Simms, Annabel E. Paton, Julian F. R. Pickering, Anthony E. Allen, Andrew M.
Copyright Year	2009
Abstract	Sympathetic nerve activity (SNA) is elevated in established hypertension. We tested the hypothesis that SNA is elevated in neonate and juvenile spontaneously hypertensive (SH) rats prior to the development of hypertension, and that this may be due to augmented respiratory–sympathetic coupling. Using the working heart–brainstem preparation, perfusion pressure, phrenic nerve activity and thoracic (T8) SNA were recorded in male SH rats and normotensive Wistar–Kyoto (WKY) rats at three ages: neonates (postnatal day 9–16), 3 weeks old and 5 weeks old. Perfusion pressure was higher in SH rats at all ages reflecting higher vascular resistance. The amplitude of respiratory-related bursts of SNA was greater in SH rats at all ages (P < 0.05). This was reflected in larger Traube–Hering pressure waves in SH rats (1.4 ± 0.8 versus 9.8 ± 1.5 mmHg WKY versus SH rat, 5 weeks old, n= 5 per group, P < 0.01). Recovery from hypocapnic-induced apnoea and reinstatement of Traube–Hering waves produced a significantly greater increase in perfusion pressure in SH rats (P < 0.05). Differences in respiratory–sympathetic coupling in the SH rat were not secondary to changes in central or peripheral chemoreflex sensitivity, nor were they related to altered arterial baroreflex function. We have shown that increased SNA is already present in SH rats in early postnatal life as revealed by augmented respiratory modulation of SNA. This is reflected in an increased magnitude of Traube–Hering waves resulting in elevated perfusion pressure in the SH rat. We suggest that the amplified respiratory-related bursts of SNA seen in the neonate and juvenile SH rat may be causal in the development of their hypertension.
Related Links	http://dx.doi.org/10.1113/jphysiol.2008.165902
Ending Page	610
Page Count	14
Starting Page	597
File Format	PDF
ISSN	00223751
e-ISSN	14697793
Journal	The Journal of Physiology
Issue Number	Pt 3
Volume Number	587
Language	English
Publisher	Blackwell Science Inc
Publisher Date	2009-02-01
Access Restriction	Open
Rights Holder	Blackwell Science Inc
Subject Keyword	Physiology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Physiology Sports Science

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Amplified respiratory-sympathetic coupling in the spontaneously hypertensive rat: does it contribute to hypertension?

Respiratory-related discharge pattern of sympathetic nerve activity in the spontaneously hypertensive rat.

Does enhanced respiratory–sympathetic coupling contribute to peripheral neural mechanisms of angiotensinII–salt hypertension?

Hypertension is critically dependent on the carotid body input in the spontaneously hypertensive rat

Does the median preoptic nucleus contribute to sympathetic hyperactivity in spontaneously hypertensive rats?

Effects of chronic hypertension and sympathetic nerves on the cerebral microvasculature of stroke- prone spontaneously hypertensive rats.

Is carotid body input the only critical mechanism involved in hypertension in spontaneously hypertensive rat?

Does enhanced respiratory-sympathetic coupling contribute to peripheral neural mechanisms of angiotensin II-salt hypertension?

Circumventricular Organ Apelin Receptor Knockdown Decreases Blood Pressure and Sympathetic Drive Responses in the Spontaneously Hypertensive Rat

Amplified respiratory–sympathetic coupling in the spontaneously hypertensive rat: does it contribute to hypertension?

Similar Documents

Amplified respiratory-sympathetic coupling in the spontaneously hypertensive rat: does it contribute to hypertension?

Respiratory-related discharge pattern of sympathetic nerve activity in the spontaneously hypertensive rat.

Does enhanced respiratory–sympathetic coupling contribute to peripheral neural mechanisms of angiotensinII–salt hypertension?

Hypertension is critically dependent on the carotid body input in the spontaneously hypertensive rat

Does the median preoptic nucleus contribute to sympathetic hyperactivity in spontaneously hypertensive rats?

Effects of chronic hypertension and sympathetic nerves on the cerebral microvasculature of stroke- prone spontaneously hypertensive rats.

Is carotid body input the only critical mechanism involved in hypertension in spontaneously hypertensive rat?

Does enhanced respiratory-sympathetic coupling contribute to peripheral neural mechanisms of angiotensin II-salt hypertension?

Circumventricular Organ Apelin Receptor Knockdown Decreases Blood Pressure and Sympathetic Drive Responses in the Spontaneously Hypertensive Rat

Amplified respiratory–sympathetic coupling in the spontaneously hypertensive rat: does it contribute to hypertension?