The first article in this issue by Sarikonda and colleagues is an excellent, up-to-date, and timely review of the major animal models of hypertension. These are described in detail in terms of the mechanisms that they incorporate and emphasize similarities and differences with human forms of hypertension. The majority of these models are produced by stimulating renal production of renin or salt and water retention as well as by involving other humoral factors. Some of the more sophisticated transgenic and gene knockout models, while interesting, have not yet been demonstrated to have close human parallels. Perhaps future findings will make these models more directly relevant to man.
Gingras et al call our attention to the rarely considered role of the adventitial layer of conduit vessels and the changes in both structure and function that they undergo as a precursor to hypertension and cardiovascular disease (CVD). This elegant review is well worth reading and should provide new areas of research.
The inflammatory marker, C-reactive protein (CRP), is acknowledged to be involved in vascular disease and to increase in forms of hypertension induced by angiotensin II. Ortiz and associates studied the role of mineralocorticoid receptor antagonism on this action and found a decrease in both plasma and urinary CRP by blocking this receptor. In addition to suggesting the potential for using urinary CRP as a method of measuring this factor, these findings further confirm a role for aldosterone in mediating the angiotensin II-induced inflammatory response and vascular damage.
Heflin and colleagues have applied very complex and sophisticated hydraulic modeling programs to the hemodynamic challenges posed by renal artery aneurysms and renal vascular hypertension. They have established critical changes in pressure and flow across these structures that impact changes in renal blood flow and pressure leading to blood pressure (BP) elevation.
Vigil and associates measured cystatin C, known to be associated with renal and CVD, in a large hypertensive population and found it to be increased in subjects with metabolic syndrome and obesity. This provides additional information regarding identification of high-risk individuals and, potentially, new therapeutic approaches to them.
Fonarow et al, examines the relative effects of long-acting carvedilol or metoprolol on insulin sensitivity and lipids in over 500 nondiabetic hypertensives not receiving lipid therapy by randomly assigning them to these agents with a titration sequence to the same target BP. They found no differences in high-density lipoprotein (HDL) levels in the 2 groups but higher triglycerides in the metoprolol group and lower insulin and C-peptide levels in the carvedilol group. In view of the dual alpha- and beta-adrenergic blockade of the latter drug and the long-recognized beneficial effects of alpha blockade on lipids and insulin sensitivity, these results are not surprising, but have immense clinical relevance.
The final paper by Mulazzi and associates presents the results of a 6-question instrument administered to a large population of high-risk hypertensives in an outpatient setting to identify factors associated with poor medication adherence thought to be the cause of their poor BP control. They identified age, male gender, diabetes mellitus, peripheral artery disease and alcohol consumption as such factors. It will be interesting to learn whether this information can be used to devise strategies for improving adherence, and BP control and for reducing cardiovascular events.
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