ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1991.tb01368.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

SUMMARY1. The normal structural adaptation of heart and vessels to regional changes in load or/and tissue demands is surveyed with respect to its importance for cardiovascular function in normotension as well as in physiological (giraffes) and pathophysiological (e.g. human and rat primary hypertension) variants of high pressure states.2. At the local level it implies an entirely appropriate adjustment of cardiovascular geometric design according to principles inherent in the LaPlace and Poiseuille laws. However, when generalized to all systemic circuits, as in primary hypertension, it invites to a potentially dangerous positive feedback interaction with even ordinary functional pressor influences.3. It is further emphasized how resistance vessels, besides the obvious influence of changes in: (i) vascular smooth muscle activity, are greatly affected also by changes of their (ii) geometric design, (iii) wall distensibility, and (iv) transmural pressure, how each of these four parameters can be independently altered and how they interact. Genetic reinforcements and various trophic influences may facilitate the extent and rate of ‘structural upward resetting’ in primary hypertension, and this resetting also encompasses the barostat mechanisms.4. Against such a background it is, in fact, from a physiological point of view, more difficult to explain how 85–90% of the population manage to maintain lifelong normotension than to explain why hypertension gradually afflicts the remaining 10–15%. It points to the presence of potentially powerful and durable, negative feedbacks that are still poorly understood (e.g. Muirhead's renomedullary depressor system).5. Considering the dominant haemodynamic influence of the structural factor in primary hypertension, it is finally stressed how the long‐range goal of antihypertensive treatment should be to cause full regression of the structural upward resetting, or perhaps even to prevent its early development in subjects predisposed for hyp

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1991.tb01369.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

SUMMARY1. The relationship between essential hypertension and abnormalities of the proximal resistance vessels (small arteries) is reviewed, with particular emphasis on their structure.2. There seems to be good evidence that the media: lumen ratio of these vessels is increased, and this may account for the increased pressor response.3. Whether there is also growth is not clear, and it is possible that the altered structure is due to redistribution of existing cells.4. Regardless of the basis for the altered structure, it appears that in essential hypertension the altered vascular structure is in itself sufficient to explain the increased peripheral resistance.5. Paradoxically, the altered vascular structure does not seem to be the main determinant of blood pressure, but the altered vascular structure appears to allow it to perform its function in the most convenient fashion.6. It is suggested that the interest in vascular structure lies in connection with therapy, for correction of blood pressure without correction of vascular structure will probably not prevent all the consequences of the disease.7. Current therapies do not appear to be able, in the short‐term, to normalize vascular structure, indicating that there is a need to find other more specific ways of correcting vascular structur

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1991.tb01370.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

SUMMARY1. A brief review is presented which summarizes the role of the kidney in the long‐term regulation of arterial pressure and the mechanism whereby changes in body fluid volume can influence the function and structure of the systemic vasculature.2. Studies indicate that the kidney detects changes of arterial pressure via changes of medullary blood flow which in the volume expanded state is poorly autoregulated. Elevations of renal arterial pressure raise vasa recta capillary pressure and renal interstitial fluid pressure, which in turn reduces tubular reabsorption of sodium and water.3. The sensitivity of the pressure–diuresis relationship is controlled by renal sympathetic nerve activity and a variety of hormone and autocrine systems.4. Evidence is also reviewed which shows that small changes of blood volume (5%) resulting from reduced renal excretion can acutely and chronically result in 25% increases of total peripheral resistance and arterial pressure.5. Short‐term increases of vascular resistance are predicted by regional autoregulatory responses while long‐term elevations of vascular resistance appear to result from the structural changes of large vessel hypertrophy and microvascular rarefaction within skeletal

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1991.tb01371.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

SUMMARY1. Evidence from experiments in conscious, instrumented dogs shows that hypertension from renal artery stenosis is due to: (i) the stimulus, the mechanical resistance of the stenosis; and (ii) the secondary responses to this, especially angiotensin II (initially) and cardiovascular hypertrophy.2. The hydraulic resistance of the stenosis is responsible for about 20–25% of the rise in blood pressure.3. Angiotensin II is initially the most important secondary response to the stenosis. Within days, however, other as yet undetermined factors become dominant in the maintenance of the hypertension. The most important of these factors is probably cardiovascular hypertrophy.4. These secondary factors are homeostatic, in that they mitigate the effects of stenosis on renal functio

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1991.tb01372.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

SUMMARY1. In animal experiments, acetylcholine is generally a vasodilator acting indirectly by releasing endothelium‐derived relaxing factor (EDRF); for example, in dog and rabbit small coronaries mounted in a myograph, acetylcholine caused concentration‐dependent relaxation.2. In human small coronary arteries taken from the atrial appendage, however, acetylcholine caused concentration‐dependent contraction with a funcionally intact endothelium as shown by the relaxation in response to substance P, another stimulant of EDRF release.3. We propose that coronary microvessels from various species have variable populations of acetylcholine receptors on the medial smooth muscle that cause contraction and on the endothelium that cause the release of EDRF. In humans, the medial smooth muscle receptors appear to predominate, and may thus play a role in coronary vasoconstri

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1991.tb01373.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

SUMMARY1. Hypertrophy of vascular and cardiac smooth muscle is present in human primary hypertension. The amplifier properties associated with hypertrophy play a major role in maintaining hypertension.2. Long‐term antihypertensive drug therapy causes substantial regression of the structural changes, assessed by the non‐autonomic component of vascular resistance, and by left ventricular mass. The latter occurs more slowly.3. The more complete the reversal of left ventricular hypertrophy, the more slowly hypertension redevelops if long‐term antihypertensive therapy is discontinued.4. Subjects who redevelop hypertension more rapidly tend to have higher cardiac output, suggesting that the cardiac amplifier may play a role in the pathogenesis.5. Studies of small arteries and of veins from patients with primary hypertension suggest that there may be a general disturbance of vascular smooth muscle function, independent of the mechanical effects of elevated systemic blood pre

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1991.tb01374.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

SUMMARY1. Anoxic perfusion of the isolated rat heart releases noradrenaline in the absence of sympathetic nerve fibre stimulation.2. Anoxic noradrenaline release is enhanced by reducing the extracellular Na+ concentration, consistent with the proposal that such release occurs by carrier‐mediated efflux.3. Release is also enhanced by lignocaine but inhibited by amiloride and ethylisopropylamiloride, suggesting that sodium entry into adrenergic nerve terminals during anoxia occurs by Na+/H+ (and possibly Na+/Ca2+) exchang

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1991.tb01375.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

SUMMARY1. The effects of neuropeptide Y (NPY) and related peptide fragments on blood pressure and vagal action at the heart were compared in the anaesthetized rat.2. A change in vagal action was taken as a measure of presynaptic activity and a change in blood pressure was taken as a measure of postsynaptic activity.3. NPY, NPY‐(13‐36) and a stabilized 13‐36 analogue of NPY (ANA NPY) all exerted pressor actions and attenuated vagal action at the heart.4. On the basis of different potencies demonstrated for the pressor and vagal inhibitory actions of these peptides, the results are consistent with the proposal that there are two populations of NPY rece

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1991.tb01376.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY

摘要:

SUMMARY1. The cardiovascular actions of central noradrenergic (NA) neurons was examined using the acute neurotransmitter releasing actions of intracisternal 6‐hydroxydopamine in conscious rabbits.2. The predominant actions of NA pathways in the brain‐stem are to inhibit vasomotor and cardiac sympathetic activity and to facilitate cardiac vagal responses.3. NA projections to the spinal cord tonically inhibit vasoconstrictor tone and form part of a high gain control system for responding to changes in specific afferent information.4. The forebrain NA projections influence heart rate through modulation of the baroreflex gain of the cardiac vagus.5. Central antihypertensive drugs such as clonidine and α‐methyldopa mimic most of the brain‐stem actions of the central NA neurons. They also utilize the ascending NA pathways influencing the baroreflex vagal gain to minimize the baroreflex effects of reducing mean arterial pressure.6. Thus, NA neurons influence the circulatory system through actions at all levels of the central nervous system and provide a comprehensive framework for integrating cardiovascular information from multiple inputs. This provides a number of targets for future development of useful pharmacologica

ISSN:0305-1870    

DOI:10.1111/j.1440-1681.1991.tb01377.x

出版商:Blackwell Publishing Ltd    

年代:1991

数据来源: WILEY