Thickening and narrowing of resistance arteries must, by definition, be key elements in the control of the cardiovascular system. However, the precise location of resistance arteries is difficult to establish. This is due to technical problems related to the small size of the vessels, to the measurement conditions disturbing the hemodynamics, and to the status of the animals while the measurements are being made. Furthermore, due to large data heterogeneity, previous studies do not give unequivocal information concerning the pressure profile in the vascular system, or the level of arterial diameter responsible for blood flow. Finally, and importantly, there is little evidence regarding the conscious state, which is thus a major limitation to understanding the mechanisms of blood distribution and the pathogenesis for disease processes such as genetic hypertension. This review first summarizes briefly the techniques which are available for identifying resistance arteries and the inherent technical limitations which are involved. The review then provides a critical assessment of the available data, both as regards measurement of local blood pressures and as regards control of peripheral resistance. The evidence suggests that, at least as regards rats and other small animals, feed arteries as well as more distal microvessels contribute to the maintenance and regulation of blood flow and resistance. Evidence from larger animals is however lacking, and it is thus unclear if resistance function should be based on arterial diameter or anatomic location. Furthermore, evidence concerning man is not available. We therefore conclude the review with suggestions for future research in this area.

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 (P_mes) was 86% of systemic pressure (P_sys). After recovering from the anaesthetic, 6-8 h later, while P_sys rose from average 79 to 114.5 mm Hg, P_mes /P_sys fell to 69%. By contrast, when anaesthesia was induced, although P_sys immediately fell by 44%, P_mes/P_sys 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 P_sys was unaffected, P_mes/P_sys fell from 67 to 27%. Conversely, with noradrenaline, P_sys rose by 30%, but P_mes/P_sys remained unchanged. Angiotensin-II showed a third pattern, where P_sys increased by 38%, but P_mes/P_sys 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.

Abnormal resistance artery structure independently predicts cardiovascular events in essential hypertensive patients at moderate risk.

No abstract

Correction of structural abnormalities in resistance arteries of patients with essential hypertension is a potential treatment goal, in addition to blood pressure reduction. However, available evidence from human as well as from animal studies indicates that antihypertensive therapy is not always accompanied by normalization of resistance vessel structure, despite normalization of blood pressure. Thus, blood pressure is not the only factor determining resistance vessel structure, and experimental studies show that several factors could play a role, including shear stress and hormonal stimulation. To date, there has been no systematic review of the many published papers which have studied the structural effects of antihypertensive therapy, and it is not known which conditions are best able to normalize resistance vessel structure. We have therefore made a survey of the available literature. The survey shows that change in blood pressure in indeed a poor indicator of change in resistance vessel structure. However, it is a remarkably consistent finding that normalization of resistance vessel structure is obtained with therapeutic regimens which reduce blood pressure by vasodilation rather than by lowering cardiac output Thus, to the extent that normalization of resistance vessel structure is deemed a goal of antihypertensive treatment, the survey points towards the importance of considering not only the treatment effect on blood pressure, but also the haemodynamic effects within patients with essential hypertension.

Our study shows no increased risk of hypertension with exposure to noise in the lower half of the 80-90 dB(A) range.

Background:Renal denervation (RDN), treating resistant hypertension, has, in open trial design, been shown to lower blood pressure (BP) dramatically, but this was primarily with respect to office BP.Method:We conducted a SHAM-controlled, double-blind, randomized, single-center trial to establish efficacy data based on 24-h ambulatory BP measurements (ABPM). Inclusion criteria were daytime systolic ABPM at least 145 mmHg following 1 month of stable medication and 2 weeks of compliance registration. All RDN procedures were carried out by an experienced operator using the unipolar Medtronic Flex catheter (Medtronic, Santa Rosa, California, USA).Results:We randomized 69 patients with treatment-resistant hypertension to RDN (n = 36) or SHAM (n = 33). Groups were well balanced at baseline. Mean baseline daytime systolic ABPM was 159 ± 12 mmHg (RDN) and 159 ± 14 mmHg (SHAM). Groups had similar reductions in daytime systolic ABPM compared with baseline at 3 months [−6.2 ± 18.8 mmHg (RDN) vs. −6.0 ± 13.5 mmHg (SHAM)] and at 6 months [−6.1 ± 18.9 mmHg (RDN) vs. −4.3 ± 15.1 mmHg (SHAM)]. Mean usage of antihypertensive medication (daily defined doses) at 3 months was equal [6.8 ± 2.7 (RDN) vs. 7.0 ± 2.5 (SHAM)].RDN performed at a single center and by a high-volume operator reduced ABPM to the same level as SHAM treatment and thus confirms the result of the HTN3 trial.Conclusion:Further, clinical use of RDN for treatment of resistant hypertension should await positive results from double-blinded, SHAM-controlled trials with multipolar ablation catheters or novel denervation techniques.

Abstract-Hypertension is associated with reduced coronary vasodilatory capacity, possibly caused by structural changes in the coronary resistance vessels. Because vasodilatory treatment may correct abnormal structure better than nonvasodilating treatment, we compared whether long-term angiotensin-converting enzyme (ACE) inhibition has a greater effect on coronary reserve and cardiovascular structure than ␤-blockade in patients with essential hypertension. Thirty previously untreated hypertensive patients were randomized in a double-blind design to treatment for 1 year with either perindopril (4 to 8 mg per day, nϭ15) or atenolol (50 to 100 mg per day, nϭ15) and furthermore compared with normotensive controls. Cardiac output and left ventricular mass were measured with echocardiography and resistance artery structure was determined in vitro. Using positron emission tomography, myocardial perfusion (MP) was determined at rest and during dipyridamole-induced hyperemia while still on medication. Perindopril reduced left ventricular mass by 14Ϯ4% (PϽ0.01), peripheral vascular resistance by 12Ϯ6% (PϽ0.01), and media thickness-tolumen diameter ratio of resistance arteries by 16Ϯ4% (PϽ0.05), whereas atenolol had no effect.