Low-income Spanish-speaking Hispanics are receptive to participate in diabetes-related research. This study shows that the pilot-tested diabetes self-management program is promising and warrants the conduct of a randomized clinical trial.

Serum uric acid independently predicted blunted renal vascular responsiveness to Ang II, consistent with results from experimental hyperuricemia showing an activated intrarenal RAS. This could be due to a direct effect of uric acid or reflect a more fundamental renal process. These data may have relevance to the association of uric acid with risk for hypertension and nephropathy.

Abstract-Experimental evidence supports a causative role for uric acid in the pathogenesis of hypertension. Prospective studies have variably adjusted for relevant confounders and have been of relatively limited duration. We prospectively examined the relationship between uric acid level and the development of hypertension in the Normative Aging Study, a longitudinal cohort of healthy adult men. Key Words: uric acid Ⅲ hypertension Ⅲ renal function Ⅲ prospective studies Ⅲ aging T he association of hyperuricemia with hypertension has long been recognized. 1 It remains unresolved whether the association of hyperuricemia with hypertension is solely because of underlying renal and metabolic abnormalities. Decreased renal blood flow 2 and decreased tubular secretion of uric acid 3 have been associated with hyperuricemia in hypertension. Hyperinsulinemia secondary to insulin resistance may also contribute to the association of hyperuricemia with hypertension. 4,5 Recent observations in experimental hyperuricemia suggest that uric acid may in fact have a pathogenic role in hypertension. 6 Hyperuricemia induces hypertension in experimental animals that corrects with hypouricemic therapy. 7 Elevated serum uric acid level has been associated with increased risk for developing hypertension. 8 -18 The Normative Aging Study (NAS), a longitudinal study of aging begun in 1963 and with ongoing follow-up, presented a unique opportunity to examine the relationship between serum uric acid level and the development of hypertension. The duration of follow-up, Յ40 years, allowed us to assess the durability of the prospective association of uric acid level with hypertension. The comprehensive data collection allowed adjustment for key potential confounding covariates, such as central adiposity, alcohol intake, metabolic parameters, and, in a subset of study subjects, the serum creatinine level. Previous studies have variably accounted for these confounders. Specifically, some did not adjust for blood pressure, 8,9,17,18 Ն2 elements of the metabolic syndrome, 8 -11,13-15 or alcohol intake, 11,12 and only 1 adjusted for renal function. 13 We, therefore, examined the prospective association of serum uric acid level with the development of hypertension among subjects at risk for the development of hypertension within the NAS cohort, including an analysis of those at risk for the development of hypertension at the time of their first serum creatinine determination. We have included in our multivariable model(s) covariates of the metabolic syndrome, alcohol intake, and renal function. MethodsSubjects were participants in the NAS, a longitudinal study of aging established by the Veterans Administration in 1961. 19 The study cohort consists of 2280 community-dwelling men from the greater Boston area who were 21 to 80 years of age on enrollment. Volunteers were screened at entry according to specific health criteria and were free of known chronic medical conditions at the

Overt and subclinical hypothyroidism are associated with increased systemic vascular resistance and hypertension. We examined the relationship between thyroid function and blood pressure homeostasis in euthyroid individuals. A total of 284 subjects (68% hypertensive) consumed high- (200 mmol) and low- (10 mmol) sodium diets, and their blood pressure responses were assessed as percentage change in the mean arterial pressure (MAP). p-Aminohippuric acid clearance was used to estimate effective renal plasma flow. Renal vascular resistance (RVR) was calculated as MAP divided by effective renal plasma flow. Serum free T(4) index (FTI) was lower (P < 0.0001) and TSH was higher (P = 0.046) in hypertensive compared with normotensive subjects independent of other baseline characteristics. FTI (beta = -1.51, P < 0.0001), baseline MAP, and race independently predicted MAP salt sensitivity. The FTI relationship with salt sensitivity adjusted for baseline MAP and race was similar among normotensive (beta = -1.42, P = 0.008) and hypertensive subjects (beta = -1.66, P = 0.0001). FTI correlated negatively with high- (P = 0.0001) and low- (P = 0.008) salt RVR, whereas TSH correlated positively with high- (P = 0.016) and low- (P = 0.012) salt RVR independent of age, gender, race, and body mass index. We have found that FTI is lower and TSH is higher in hypertensive compared with normotensive euthyroid subjects and that FTI independently predicts blood pressure salt sensitivity. These data show that the influence of thyroid function on blood pressure homeostasis extends into euthyroid range and likely reflects the action of thyroid hormone on peripheral vasculature.

Accumulating evidence suggests that genes of the hypothalamic-pituitary-thyroid pathway influence susceptibility to hypertension. Type 2 iodothyronine deiodinase is responsible for the conversion of thyroxine to tri-iodothyronine for use in peripheral tissues. The present study evaluated whether a type 2 iodothyronine deiodinase nonsynonymous polymorphism, threonine 92 to alanine (Thr92Ala), is a determinant of hypertension susceptibility. A total of 372 euthyroid subjects were genotyped for Thr92Ala polymorphism using the Sequenom MassARRAY platform. Associations with hypertension and hypertension-related intermediate phenotypes were performed with generalized estimating equations. Type 2 iodothyronine deiodinase Thr92Ala allele frequencies differed significantly between hypertensive and normotensive subjects, with an excess of Ala92 carriers in hypertensive compared with normotensive subjects (64.8% versus 47.1%; P=0.011). Adjusted for age, gender and race, the estimated odds ratio for hypertension in Ala92 allele carriers compared with Thr92 homozygotes was 2.11 (95% CI: 1.15 to 3.89). Among euthyroid adults, the common Ala92 allele of the type 2 iodothyronine deiodinase increases risk for the development of hypertension. These data support an important role for genetic variation in the hypothalamic-pituitary-thyroid pathway in influencing susceptibility to hypertension.

There is familial aggregation of high-normal TSH values in hypertensive families, and a hypertension family history influences serum TSH levels in healthy individuals. These findings are consistent with the existence of genetic variants affecting both blood pressure regulation and serum TSH levels.

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Accumulating evidence indicates that aldosterone is involved in cardiovascular disease by inducing inflammation in the presence of moderate amounts of salt in the diet. Spironolactone and eplerenone are the mineralocorticoid receptor (MR) antagonists currently available for the treatment of hypertension. They have similar safety and antihypertensive efficacy. The advantage of eplerenone is the lower incidence of anti-androgenic and progestational side effects. The rationale for using MR blockade in the treatment of hypertension is threefold: the evidence of antihypertensive efficacy, the phenomenon of "aldosterone escape" occurring with angiotensin-converting enzyme inhibitor and angiotensin-receptor blockade therapy, and the compelling evidence that MR antagonism reduces target-organ damage in hypertensive patients and improves survival in patients with cardiovascular disease. Thus, blockade of the MR may be very useful in many patients with hypertension, particularly those at risk for or having evidence of target-organ damage.