This brief review summarizes the author’s current understanding of the circulatory changes in hypertension. Differences in four important regulatory systems are dependent on structural changes: (1) An increase in wall-to-lumen ratio of precapillary resistance vessels is responsible for an increase in vascular reactivity, or ‘structural autoregulation’. (2) A structural change primarily in the preglomerular arteriole causes a resetting of the pressure required for glomerular filtration. This serves a ‘long-tem barostatic function’. (3) Stiffening of the aorta and other pressure-sensing systems contributes to a resetting of baroreceptors bringing about a reset of the ‘short-term barostats’. (4) Left ventricular hypertrophy causes a decrease in compliance, hence tending to decrease stroke volume for a given filling pressure. Functional changes such as increased neurogenic activity may serve as important ‘trigger’ elements in spontaneously hypertensive rats and at least in one important variant of essential hypertension in the human. An example of a functional alteration in vascular smooth muscle is found in that the vascular resistance response in the spontaneously hypertensive rat in low calcium concentration (0.2 mM) is better maintained than in the normotensive control rat, but this alteration seems to be secondary in nature. An experiment is described which permits simultaneous assessment of the responses of capacitance and resistance vessels to nerve stimulation: when the splanchnic nerves are stimulated there is a simultaneous decrease in venous capacity and an increase in resistance in the liver, gastrointestinal tract and kidneys. The decrease in venous capacity is reflected in an increase in stroke volume whereas the increase in regional resistance is evidenced in an incraese in total peripheral resistance. Using this index the spontaneously hypertensive rats had a less efficient capacitance response (possibly due to the decrease in ventricular compliance) and a greater resistance response than did the normotensive control rat. Although both functional and structural changes in the cardiovascular system occur, the rapidly developed structural changes appear to be the major determinant of the differences between normal and hypertensive hemodynamics.

Keywords:
Hypertension, Nervous cardiovascular control, Spontaneously hypertensive rats, Structural vascular changes, Vascular reactivity, Vascular resistance, Vascular smooth muscle
This content is only available via PDF.
© 1978 S. Karger AG, Basel
1978
Copyright / Drug Dosage / Disclaimer
Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.
Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.
You do not currently have access to this content.