The small arteries (prearteriolar vessels with lumen diameter less than approximately 500 microns) contribute importantly to and participate actively in the regulation of the peripheral resistance. New techniques, building on the classic histological and hemodynamic techniques, have enabled detailed in vitro investigation of small arteries. At present, research in small arteries is in its infancy, and our understanding of the heterogeneity of small arteries within vascular beds, between vascular beds, and between species is extremely limited. This review attempts to describe the current status of the field. New techniques, based primarily on a wire myograph (where the vessels are mounted as ring preparations) and a pressure myograph (where vessels are cannulated and pressure-lumen relations are determined), have allowed in vitro investigations of small arteries. The more physiological arrangement of the pressure myograph allows, for example, investigation of the vasoconstrictor response to raised intravascular pressure (the Bayliss response), whereas the less-sophisticated wire myograph is similar to use and may be more useful in certain situations where particular mechanisms are being investigated. Both techniques allow simultaneous measurements of vessel tone and a variety of parameters (e.g., membrane potential and intracellular ion activities) and thus allow precise determination of the relation between small artery structure and function. The vessels appear to remain fully viable with regard to the contractility of their smooth muscle cells as well as to the function of their perivascular nerves and their endothelium. The evidence suggests that the monovalent transport mechanisms in the plasma membrane, in particular potassium channels, play an important role in the determination of the membrane potential in small arteries, although the relation is more complex than indicated by the Goldman equation. Confirmation of these findings requires, however, simultaneous determinations of ion transport and vascular tone under conditions where vessels are subjected to mechanical loading. The membrane potential, through its effect on potential-dependent calcium channels, plays an important role in the determination of vascular tone. With regard to calcium homeostasis, current knowledge is hampered by the lack of direct measurements of the relation between cytoplasmic calcium and vascular tone. The evidence, however, suggests that besides potential-dependent calcium channels, receptor-operated calcium channels are present in the plasma membrane, although this still requires confirmation. The role of the sarcoplasmic reticulum is not clarified.(ABSTRACT TRUNCATED AT 400 WORDS)
Growth or altered metabolism of nonmyocyte cells (cardiac fibroblasts, vascular smooth muscle and endothelial cells) alters myocardial and vascular structure (remodeling) and function. However, the precise roles of circulating and locally generated factors such as angiotensin II, aldosterone and endothelin that regulate growth and metabolism of nonmyocyte cells have yet to be fully elucidated. Trials of pharmacologic therapy aimed at preventing structural remodeling and repairing altered myocardial structure to or toward normal in the setting of hypertension, heart failure and diabetes are reviewed. It is proposed that these are therapeutic goals that may reduce cardiovascular morbidity and mortality. Although this hypothesis remains unproved the primary goal of therapy should be to preserve or restore tissue structure and function.
This paper describes a new technique for determining the intravascular pressure at the base of mesenteric arcades (arterial diameter less than 200 µm) in conscious, unrestrained, resting rats, using this technique we found that under Brietal anaesthesia, shortly after implanting the catheters, the pressure in the base of the arcades (Pmes) was 86% of systemic pressure (Psys). After recovering from the anaesthetic, 6-8 h later, while Psys rose from average 79 to 114.5 mm Hg, Pmes /Psys fell to 69%. By contrast, when anaesthesia was induced, although Psys immediately fell by 44%, Pmes/Psys did not change. Acute pharmacological experiments in resting animals showed that the relative contribution of the arcade vessels to the peripheral resistance was variable. When serotonin was injected into the aorta, although Psys was unaffected, Pmes/Psys fell from 67 to 27%. Conversely, with noradrenaline, Psys rose by 30%, but Pmes/Psys remained unchanged. Angiotensin-II showed a third pattern, where Psys increased by 38%, but Pmes/Psys rose transiently to 86%. The data suggest that in the rat mesenteric bed, under conscious conditions, the arcade arteries can contribute substantially to the control of peripheral resistance.
The structure of the resistance vessels is altered (remodeled) in individuals with high blood pressure (essential hypertension). The structure is dependent not only on blood pressure but also on blood flow and hormonal environment. Vascular biology is providing increased knowledge of the mechanisms involved and thus contributing to our understanding of the pathophysiology of the disease.
The myogenic response of small arteries and arterioles has been shown to contribute significantly to autoregulation in different vascular beds. It is characterized by a constriction of the vessel after an increase of transmural pressure and a dilation of the vessel after a decrease of transmural pressure. This review examines the evidence for the mechanisms of the myogenic response, with the aim of distinguishing between facts and hypotheses. It appears to be established that the myogenic response is stimulated by an alteration of vessel wall tension, that it does not require the presence of the endothelium and, for pressure increases, that it is accompanied by a membrane depolarization and an increase of the intracellular Ca2+ concentration, which depends largely on an influx of extracellular calcium via voltage-operated calcium channels. Under in vitro conditions, it may further be considered an established fact that the myogenic response can be modulated by transmitters, like noradrenaline, and factors released from the endothelium upon its activation. In contrast, many other aspects of the myogenic response remain hypothetical. Thus, the mechanism of the depolarization, its importance for the development of the myogenic response, the participation of other pathways for calcium influx, and the role of an intracellular calcium release in the myogenic response are still under debate. Furthermore, the participation of a variety of intracellular second messenger systems in the myogenic response, i.e. inositol trisphosphate, diacylglycerol, phospholipase A2, protein kinase C or 20-hydroxyeicosatetraenoic acid, is still unclear. Additionally, the roles of the pulsatility of the blood pressure and of remote signals from neighbouring vessel segments as well as of different metabolites are not clarified. This review suggests that while the primary mechanisms of the myogenic response are well understood, the details of the signalling pathways are still undefined. The clinical significance of the myogenic response remains to be determined.
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The structure of the resistance vessels is altered (remodeled) in individuals with high blood pressure (essential hypertension). The structure is dependent not only on blood pressure but also on blood flow and hormonal environment. Vascular biology is providing increased knowledge of the mechanisms involved and thus contributing to our understanding of the pathophysiology of the disease.
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