Neurogenic hypertension. A new MRI protocol for the evaluation of neurovascular compression of the cranial nerves IX and X root-entry zone.

OBJECTIVE: Neurovascular compression of the rostral ventrolateral medulla (RVLM) has been implicated in the pathogenesis of essential hypertension. Although MRI has been widely used to evaluate the morphologic relation of structures in this region, spatial resolution of the previously used techniques was limited. This article describes the use of a new MRI protocol that combines two sequences with improved spatial resolution and complementary image information as well as a set of defined criteria for image analysis. METHODS: MRI of the brain stem was performed in 60 hypertensive and 50 normotensive subjects using a 3D-CISS and a 3D-FISP-MRA sequence. Neurovascular contact in the RVLM was independently assessed by four readers using predefined criteria and compared with a consensus finding. Agreement was expressed by kappa statistics on a 0 to 1 scale. RESULTS: Left-sided neurovascular contact within the RVLM was found in 13 (22%) hypertensive and 6 (12%) control subjects. The inter-reader agreement for positive and negative findings ranged from 0.47 to 0.79; agreement to the consensus finding ranged from 0.65 to 0.90. CONCLUSIONS: The combination of 3D-CISS and arterial flow-sensitive 3D-FISP, together with the evaluation criteria defined in this study, can be used for describing the finer anatomic features of the brain stem, and in particular for investigation of neurovascular contact of the IX/X cranial nerve root-entry zone. The high quality of images and the substantial or almost perfect reader-consensus agreement should make this protocol useful for future investigations of the neurovascular compression syndrome in patients with essential hypertension and possibly in other neurovascular compression syndromes, such as trigeminal neuralgia and hemifacial spasm.

G-Protein beta3 subunit C825T variant and ambulatory blood pressure in essential hypertension.

Recent studies have identified a novel polymorphism (C825T) of the gene encoding the beta3 subunit of heterotrimeric G proteins (Gbeta3) associated with enhanced activation of G proteins, which appears to be more common in hypertensive patients. In the present study we examine the relationship between this genetic variant and hypertension in 479 white patients with established essential hypertension recruited from the hypertension clinic of the Universitätsklinikum Benjamin Franklin in Berlin, Germany, and 1000 normotensive gender- and age-matched controls. All patients were screened for the presence of secondary hypertension and were further characterized by ambulatory blood pressure measurements performed in 295 treated and 184 untreated patients. Genotype distribution for the Gbeta3-C825T genotype in patients (CC=204, CT=224, TT=51) was significantly different from that in controls (CC=514, CT=412, TT=74; chi2=11.5, P<0.01), and the T allele was associated with an odds ratio of 1.5 (95% CI, 1.1 to 2.2) versus non-T carriers for the presence of hypertension. However, in both the whole group and the untreated subgroup, blood pressure levels between the genotypic groups were virtually identical. Furthermore, age of onset of hypertension and number of antihypertensive medications (in treated patients) were similar between the genotypic groups. Thus, while our data confirm the association between the Gbeta3-C825T variant and essential hypertension, they do not support the hypothesis that this marker is associated with more severe blood pressure in patients with already established hypertension.

Identification of a renin threshold and its relationship to salt intake in a patient with pure autonomic failure.

Animal studies have demonstrated a threshold below which renin release increases proportionally to a decrease in renal perfusion pressure. Demonstration of a similar mechanism in humans, however, has proved difficult, as any attempt to lower blood pressure below the putative renin threshold results in renin release mediated by reflex activation of the sympathetic nervous system. In this study, we report on our observations in a 71-year-old woman who presented with a 20-year history of faintness and syncope and was diagnosed as having pure autonomic failure. Graded head-up tilting resulted in a stepwise reduction in mean arterial blood pressure to a minimum of 54 mm Hg, with no signs of increased sympathetic activity. A fall in blood pressure below 80 mm Hg resulted in a distinct rise in plasma renin activity, and a similar threshold pressure was observed under both a 50- and a 100-mmol/d sodium chloride diet. Below the threshold, response to changes in perfusion pressure was proportionally greater under the 50-mmol/d diet than under a 100- or 200-mmol/d diet. These observations demonstrate that a pressure threshold for renin release at 10 to 15 mm Hg below ambient blood pressure, as described previously in animal studies, is also present in humans. The significance of this pressure-dependent mechanism of renin release for the long-term regulation of blood pressure and water and mineral balance in humans remains to be determined.

Genetic variants of the renin-angiotensin system and ambulatory blood pressure in essential hypertension.

OBJECTIVE: To examine whether the angiotensinogen M235T and angiotensin converting enzyme insertion/deletion (I/D) variants are related to the severity of hypertension in patients with established essential hypertension. DESIGN: A cross-sectional study. SETTING: The hypertension clinic of the Benjamin Franklin University Hospital, Free University of Berlin. PARTICIPANTS: Three hundred and forty-three consecutive Caucasian patients who presented with treated or untreated (n = 115) hypertension were enrolled into the study. Twenty-two patients were excluded from analysis because they had secondary hypertension. MAIN OUTCOME MEASURES: Angiotensinogen M235T and angiotensin-converting enzyme I/D genotypes, 24 h ambulatory blood pressure values, the number of antihypertensive medications administered and left ventricular dimensions assessed by two-dimensional echocardiography. RESULTS: Neither the angiotensinogen nor the angiotensin converting enzyme genotype was related significantly to the average ambulatory blood pressure and left ventricular dimensions in hypertensives. Furthermore, neither the number of antihypertensive medications administered to treated patients nor blood pressure levels in untreated patients (n = 115) differed significantly between the genotypic groups. CONCLUSIONS: These results do not support the hypothesis that the studied molecular variants of the renin-angiotensin system may represent clinically useful markers of the severity of hypertension in Caucasians with established essential hypertension.