Control of blood pressure and risk of stroke among pharmacologically treated hypertensive patients

BACKGROUND AND PURPOSE: Despite improved control of blood pressure during the last decades in the United States, a considerable proportion of treated hypertensives have not achieved target blood pressure levels. We estimated the proportion of strokes occurring among treated hypertensive patients that may be attributable to uncontrolled blood pressure. METHODS: A population-based case-control study was conducted among treated hypertensive members of Group Health Cooperative of Puget Sound. Cases were treated hypertensive patients who sustained a first fatal or nonfatal, ischemic (n=460) or hemorrhagic (n=95) stroke during 1989-1996. Controls were a random sample of stroke-free, treated hypertensive Group Health Cooperative enrollees (n=2966), similar in age to the stroke cases. Multiple measurements of blood pressure and other cardiovascular risk factors were collected from medical records. Logistic regression was used to estimate the risk of ischemic stroke and hemorrhagic stroke associated with uncontrolled blood pressure, defined as diastolic blood pressure >90 mm Hg or systolic blood pressure >140 mm Hg. The fraction of strokes attributable to uncontrolled blood pressure among treated hypertensives was calculated. RESULTS: Blood pressure was uncontrolled in 78% of ischemic stroke cases, 85% of hemorrhagic stroke cases, and 65% of controls. After adjustment for potential confounders, uncontrolled blood pressure among treated hypertensive patients was moderately associated with ischemic stroke (risk ratio=1.5 [95% CI, 1.2 to 1. 9]) and strongly related to hemorrhagic stroke (risk ratio=3.0 [95% CI, 1.7 to 5.4]). We estimated that 27% (95% CI, 11% to 39%) of the ischemic strokes and 57% (95% CI, 26% to 75%) of the hemorrhagic strokes among treated hypertensive patients were attributable to uncontrolled blood pressure. Overall, 32% (95% CI, 14% to 45%) of all strokes were attributable to uncontrolled blood pressure. CONCLUSIONS: A considerable proportion of incident strokes among treated hypertensive patients may be prevented by achieving control of blood pressure.     

Amlodipine lowers blood pressure without significant effect on cerebral blood flow in hypertensive patients with a history of stroke: a quantitative single photon emission computed tomography study

Appropriate antihypertensive therapy is important to prevent cerebrovascular disease. The purpose of the present study was to investigate the effect of such therapy on cerebral blood flow in stroke patients. Twenty hypertensive patients with a history of ischemic stroke received amlodipine 2.5 or 5 mg daily for 12 weeks. Blood pressure and cerebral blood flow as measured by ¹³³Xe single photon emission computed tomography at baseline and were compared at 12 weeks. There were statistically significant reductions in both systolic (167.0 to 140.9 mm Hg) and diastolic (97.8 to 81.8 mm Hg) blood pressures after 12 weeks of amlodipine treatment. No statistically significant effect was observed on cerebral blood flow (46.7 to 46.9 ml/100g brain/min). A weak but statistically significant change was observed in cerebellar blood flow (44.1 to 46.9 ml/100g brain/min). We concluded that amlodipine reduces blood pressure without affecting cerebral blood flow in hypertensive patients with a history of ischemic stroke. Investigation about its effect on cerebellar blood flow is mandatory.     

Hemorrhagic infarct induced by arterial hypertension in cat brain following middle cerebral artery occlusion

The purpose of this experiment was to determine whether an acute rise in brain perfusion pressure causes hemorrhagic transformation of an infarct without a reopening of the occluded artery. We raised the blood pressure of 22 cats by aortic obstruction 5-24 hours after transorbital middle cerebral artery clipping; hemorrhagic infarcts were induced in 11. Mean arterial blood pressure increased by 57.2 +/- 16.9 mm Hg (mean +/- SD) in the 11 cats with hemorrhagic infarcts and by 40.4 +/- 16.9 mm Hg in the 11 remaining cats with pale brain infarcts (p less than 0.05). Induction of hypertension increased regional cerebral blood flow in the ischemic cortical gray matter more in three cats with hemorrhagic infarcts than in seven with pale infarcts. Our results demonstrate that hemorrhagic transformation of an infarct can be induced by a rapid increase in perfusion pressure to brain tissue already exposed to focal ischemia. We also suggest that the restoration of blood flow through leptomeningeal collaterals plays an important role in the pathogenesis of hemorrhagic infarction in cases without reopening of occluded arteries.     

Longitudinal study of blood pressure and white matter hyperintensities: the EVA MRI Cohort

OBJECTIVE: To investigate the relationship between baseline hypertension and severity of white matter hyperintensities (WMH) at 4-year follow-up in a sample of subjects aged 59 to 71 years old at entry. METHODS: Subjects were participants in the Epidemiology of Vascular Ageing study, a longitudinal study on vascular aging and cognitive decline. At 4-year follow-up, 845 subjects had a cerebral MRI. MRI examinations were read by a single rater to determine the severity of WMH, ranging from absent to severe. Hypertension at each wave of the study was defined as systolic blood pressure > or =160 mm Hg, diastolic blood pressure > or =95 mm Hg, or use of antihypertensive medication. RESULTS: Hypertension at baseline was significantly associated with an increased risk of having severe WMH at 4-year follow-up. When taking into account both blood pressure levels and antihypertensive drug intake, analysis showed that the risk of having severe WMH was significantly reduced in subjects with normal blood pressure taking antihypertensive medication compared with those with high blood pressure taking antihypertensive agents. Cross-sectional relationships between hypertension and WMH at 4-year follow-up showed that the frequency of severe WMH was significantly higher in people who were hypertensive at both baseline and 4-year follow-up than those who were hypertensive only at 4-year follow-up. CONCLUSIONS: Hypertension is a major risk factor for severe WMH. Subjects taking antihypertensive drugs and who have controlled blood pressure had a reduced risk of severe WMH. Longitudinal studies are needed to investigate whether reduction of the development of WMH, by treatment and prevention of hypertension, might reduce the subsequent risk of cognitive deterioration or stroke.     

Blood pressure reduction with ECT response

A group of 48 male inpatients who responded to electroconvulsive therapy for major depression showed decreases in resting blood pressure along the course of treatment. Decreases occurred in both systolic (mean +/- SD = 8.0 +/- 17.3 mm Hg, p = .0025) and diastolic (7.4 +/- 13.2 mm Hg, p = .00030) pressures. Systolic pressure decreased by at least 20 mm Hg in 15 patients. These findings are consistent with reports that depressives show elevated plasma catecholamine levels, and that, with response to tricyclic antidepressants, their blood pressures decrease. Depression-associated blood pressure elevation might contribute to the excessive cardiac mortality of depressives; conversely, antidepressant treatment might control hypertension in some depressives.     

Hypotension as a complication of hypoglycemia leads to enhanced energy failure but no increase in neuronal necrosis

The hypothesis that arterial hypotension aggravates hypoglycemic brain damage was tested. Thirty minutes of insulin induced hypoglycemia with a flat EEG ("isoelectricity") was compared in seven series of rats. In three series of animals, the energy state of the cerebral cortex was determined at blood pressures of 140, 100 and 80 mm Hg respectively. Hypotension during hypoglycemia exacerbated cortical energy failure. In the fourth to sixth series, blood pressure was adjusted during isoelectricity to 160, 100 and 60 mm Hg, respectively. A seventh series had induced hypotension to 60 mm Hg only in the recovery period. Quantitation of neuronal death was performed in the fourth to seventh series of rats by direct visual counting of acidophilic neurons in sub-serially sectioned brains after one week survival. Although the first three series demonstrated enhanced deterioration of the cerebral energy state with lower blood pressures during hypoglycemia, the fourth to seventh series showed no augmentation of quantitated hypoglycemic neuronal necrosis. The distinct distribution of hypoglycemic brain damage, suggesting a fluid-borne toxin, was present at normal and reduced blood pressures, with no tendency toward an ischemic pattern of pathology. In spite of previously demonstrated reductions of cerebral blood flow to ischemic levels in regions with pronounced loss of autoregulation, no regional exacerbation of neuronal necrosis was seen in these brain areas. It is concluded that hypoglycemic brain damage is distinct from ischemic brain damage, and that the two insults are not additive. Furthermore, moderate hypotension to 60 mm Hg does not aggravate the damage in spite of an enhanced energy failure.     

Relationship of family history scores for stroke and hypertension to quantitative measures of white-matter hyperintensities and stroke volume in elderly males

White-matter hyperintensities (WMHI) are frequently associated with cerebrovascular risk factors in the elderly, particularly hypertension, and have been interpreted as a subclinical form of ischemic brain damage. WMHI, clinical stroke and blood pressures show significant genetic influences. The objective of this study was to determine whether a relationship exists between family history of stroke and/or hypertension in first degree relatives and WMHI in the elderly. WMHI and stroke (CVA) volumes were quantified from brain MRI performed on 414 white, male twins born between 1917 and 1927 (average age 72.3 +/- 2.9 years). WMHI, adjusted for age and head size, was significantly correlated with the family history score (r = 0.21, p < 0.001). Dividing the family history scores into quintiles revealed significant differences in WMHI by quintile mean (p < 0.05). Subjects in the highest quintile of family history score had the highest mean WMHI. Recalculation of the family history score, by only counting relatives reported to have had a clinical stroke as a positive event, revealed a nonsignificant correlation with WMHI, but the correlation of the family history score with MRI CVA volume was significant (p < 0.05). Stepwise multivariate analysis including ApoE status, current smoking status, smoking packyear history, Doppler ankle/arm blood pressure ratios, current and long term hypertensive status and current systolic and diastolic pressures indicated that the stroke/hypertension family history score was the single best predictor (p < 0.01) of WMHI volumes. Family history was not an independent predictor of CVA volume.     

Blood pressure exceeding national guidelines among women after stroke

BACKGROUND AND PURPOSE: After a transient ischemic attack or stroke, the risk for recurrence may be reduced by treatment of hypertension. The purpose of this study was to determine how commonly blood pressure exceeds national guidelines among patients who have had one of these events. METHODS: Subjects were 644 women participating in a randomized trial of estrogen for secondary stroke prevention. We measured blood pressure 1 month after the stroke or TIA while patients were under the care of their personal physicians. Among 536 patients, a second measure was made at an average of 2.9 years after the first. RESULTS: The mean age of participants was 71 years, and 73% reported a history of hypertension. At baseline, only 44% (280/644) of the women had blood pressure values within national guidelines (<140/90 mm Hg). With separate guidelines used for diabetics (<130/85 mm Hg) and nondiabetics (<140/90 mm Hg), the proportions of women within the guidelines were 27% and 44%, respectively. Overall, 39% of patients were within the diabetes-adjusted guidelines. Among patients whose blood pressure exceeded 140/90 mm Hg at first examination, 55% were still in excess at follow-up. Features associated with severe hypertension at first examination (>160/100 mm Hg) were history of hypertension, education less than college, and higher cognitive functioning. CONCLUSIONS: Blood pressure values in excess of national guidelines are common after stroke and TIA, especially among diabetic patients. Efforts to lower blood pressure control may enhance secondary prevention.     

Prevention of isolation-induced hypertension by intrahippocampal administration of a nonpeptide kappa-opioid receptor agonist.

Previous research in this laboratory showed that hypertension in the spontaneous hypertensive rat (SHR) appears to correlate to insufficient production of hippocampal dynorphins, and that blood pressure could be reduced by intrahippocampal administration of dynorphins and nonpeptide kappa agonists. The purpose of the present study was to investigate whether kappa agonists could prevent the development of hypertension in a different hypertensive model, i.e., the isolated male rat model of hypertension (IHR). Isolation of young male rats for 5-7 days in standard rat cages caused an increase in systolic blood pressure from a mean of 132 to 184 mmHg. The blood pressures of rats grouped 3 per cage remained stable. Rats received the nonpeptide kappa agonist U62, 066E, (Spiradoline, Upjohn), 10 nmoles/0.2 microl or drug vehicle bilaterally into the the hippocampus for 3 days prior to and during isolation or grouping. Animals treated with U62, 066E did not develop hypertension as compared to isolated animals treated with vehicle. The isolation procedure used in these studies appears to induce anxietal stress, as indicated by reduced time spent by the rats in the open arms of the elevated-plus maze. This time is increased by U62, 066E, suggesting that the drug possesses anxiolytic properties and may reduce hypertension in part, by blocking an anxiety/stress component. These data strengthen our previous findings that opioids in the hippocampus may be important in restraining increased blood pressure provoked by environmental stimuli such as isolation.     

Blood pressure elevations in riluzole-treated patients with amyotrophic lateral sclerosis

OBJECTIVE: To determine whether riluzole is associated with blood pressure elevations in patients with amyotrophic lateral sclerosis (ALS). BACKGROUND: Though previously reported, hypertension is not considered a frequent adverse effect of riluzole. METHODS: We reviewed data from 35 consecutive ALS patients on riluzole, and 88 randomly selected controls without and 20 patients with ALS who were not on riluzole. RESULTS: A significantly greater number of ALS patients on riluzole had blood pressure elevations (28 of 35 patients) compared to controls (26 of 88, p<0.001; 8 of 20, p = 0. 007). Median systolic and diastolic blood pressures were both significantly higher in riluzole-treated (140/86 mm Hg) than in control patients without ALS (120/70 mm Hg, p<0.001). Systolic, but not diastolic, blood pressures were significantly higher in riluzole-treated patients than in controls with ALS (126 mm Hg, p = 0.002). CONCLUSIONS: Riluzole treatment may be associated with mild blood pressure elevations. Future prospective trials of riluzole should closely assess hypertension.     

Morbidity and mortality in the Systolic Hypertension in the Elderly Program (SHEP) pilot study

The pilot study of the Systolic Hypertension in the Elderly Program was a randomized, double-blind, placebo-controlled trial of drug therapy for isolated systolic hypertension. It followed 551 elderly participants with untreated blood pressures of greater than 160/less than 90 mm Hg for an average of 34 months. Mean age of the participants was 72 years; 63% were women, and 82% were white. Pretreatment blood pressures averaged 172/75 mm Hg. Participants were randomly assigned to treatment with chlorthalidone or placebo as Step I medication. Blood pressures at annual visits averaged 141/68 and 157/73 mm Hg for the drug-treated and placebo-treated groups, respectively, with 60% and 33% of the survivors on blinded medication having systolic blood pressures of less than 160 mm Hg at their last annual visit. All-cause mortality rates for the drug-treated and placebo-treated groups were 25.4 and 22.7 deaths per 1,000 participant-years of risk, and rates for definite "first stroke" were 8.3 and 12.8 per 1,000 years of risk. Differences between groups were significant for systolic and diastolic blood pressure but not for death or stroke rates. A full-scale study has begun to determine the effects of drug therapy for isolated systolic hypertension on stroke and mortality rates.     

Blood pressure and risk of headache: a prospective study of 22 685 adults in Norway

OBJECTIVES: Prevalence studies of the association between blood pressure and headache have shown conflicting results. The aim was to analyse the relation between blood pressure and risk of headache in a prospective study. METHODS: A total of 22 685 adults not likely to have headache, had their baseline blood pressure measured in 1984-6, and responded to a headache questionnaire at follow up 11 years later (1995-7). The relative risk of headache (migraine or non-migrainous headache) was estimated in relation to blood pressure at baseline. RESULTS: Those with a systolic blood pressure of 150 mm Hg or higher had 30% lower risk (risk ratio (RR)=0.7, 95% CI 0.6-0.8) of having non-migrainous headache at follow up compared with those with systolic pressure lower than 140 mm Hg. For diastolic blood pressure, the risk of non-migrainous headache decreased with increasing values, and these findings were similar for both sexes, and were not influenced by use of antihypertensive medication. For migraine, there was no clear association with blood pressure. CONCLUSION: In the first prospective study of blood pressure and the risk of headache, high systolic and diastolic pressures were associated with reduced risk of non-migrainous headache. One possible explanation may be the phenomenon of hypertension associated hypalgesia, which probably involves the baroreflex system influencing nociception in the brain stem or spinal cord.     

Development of cardiac sympathetic and adrenal-medullary responses in borderline hypertensive rats

Borderline hypertensive (BHR) rats are the first generation offspring of a cross of spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) normotensive rats. In adulthood, BHRs have systolic blood pressures in the 140-160 mm Hg range. If subjected to chronic stress paradigms, however, BHRs develop sustained and permanent elevations in systolic blood pressure (180-200 mm Hg). In the present study, we examined the functional development of cardiac and adrenal medullary responses to reflex activation of the sympathetic nervous system in preweanling BHR and WKY rats. Pups of the two groups were injected with insulin or saline at 4, 8, 12, or 16 days of age and sacrificed 3 h later. Insulin produces an acute lowering of blood glucose which is attended by a centrally mediated increase in sympathetic activity. The induction of ornithine decarboxylase (ODC) activity in heart and the depletion of epinephrine from the adrenal medulla were biochemical indicators of functional sympathetic neurotransmission. WKY and BHR pups had similar levels of cardiac ODC activity under basal conditions and following administration of insulin. In contrast, BHRs had higher amounts of adrenal norepinephrine and epinephrine from 4 to 16 days of age and greater depletion of adrenal epinephrine following insulin administration at 8, 12 and 16 days of age. These findings indicate that BHRs have a greater capacity for catecholamine biosynthesis, storage and release in the adrenal medulla during the preweanling period compared to age-matched normotensive WKY controls. This alteration in the adrenal medulla during the preweanling period may contribute to the susceptibility of adult BHR rats to stress-induced hypertension.     

3.0T磁共振SWI在高血压脑内微出血中的应用及临床意义

目的探讨磁敏感加权成像(SWI)在高血压脑内微出血中的应用及临床意义。方法选53例高血压患者,应用3.0T MR行常规MRI和SWI序列成像检查并结合临床资料进行分析。结果32例高血压患者脑内有微出血灶,在SWI上呈点状、圆形、椭圆形低信号。总数达887个,直径为0.3mm～7.6mm。分布于皮层、皮层下和基底节区。其中17例伴发缺血性脑血管病,5例出血性腔隙性梗塞,7例伴发出血性脑血管病,3例无临床症状。结论SWI序列可敏感的显示高血压脑内微出血灶,对伴发缺血性和出血性脑血管病的诊断治疗有重要的指导价值。     

Sympathetic inhibition and attenuation of spontaneous hypertension by PVN lesions in rats

To determine whether the paraventricular nucleus (PVN) contributes to the development of hypertension in spontaneously hypertensive rats (SHR), we compared cardiovascular responses to ganglionic blockade with hexamethonium or vasopressin antagonism with dPVAVP in sham-operated or PVN lesioned SHR and Wistar-Kyoto rats (WKY). Lesions were produced electrolytically when the rats were 5 weeks old. During the next 3 weeks, tail-cuff measurements showed that the development of hypertension in SHR was inhibited, while systolic pressure in WKY was unaffected. Mean pressures recorded directly from the femoral artery at 8 weeks of age were lower in lesioned than in sham-operated SHR (141 +/- 5 vs 110 +/- 3 mm Hg, P less than 0.05), but did not differ in corresponding WKY groups (110 +/- 4 vs 112 +/- 5 mm Hg). Depressor responses to ganglionic blockade induced by i.v. injection of hexamethonium (25 mg/kg) were significantly larger in sham-operated than in lesioned SHR (-41 +/- 4% vs -28 +/- 3%, P less than 0.05). By contrast, vasopressin antagonism with dPVAVP did not alter blood pressure in all rat groups. In 24-h urine samples, excretion of vasopressin was unaffected, but that of norepinephrine was significantly reduced in lesioned SHR. These findings suggest that the PVN contributes to the development of spontaneous hypertension by sympathetic activation without increasing vasopressin secretion.     

Longitudinal study of blood pressure and stroke in over 37,000 People in China

As part of a longitudinal study performed in urban China, 37,655 subjects were evaluated for stroke risk factors, including having their blood pressure measured in a standard fashion. The cohort was followed for 3.5 years during which time 427 subjects experienced incident strokes--221 ischemic, 203 hemorrhagic, and 3 undefined. Both systolic and diastolic blood pressure were significantly related to risk of stroke and stroke type. Associations were stronger for systolic than diastolic blood pressure. These results emphasize the importance of systolic blood pressure, as opposed to diastolic, as a risk factor for stroke. In this study, the risk of stroke is increased by about 25% with each 10 mm Hg increase in systolic blood pressure.     

Systolic blood pressure within an intermediate range may reduce memory loss in an elderly hypertensive cohort.

The objective of this study was to determine if maintenance of systolic blood pressure (BP) within a high range or low range among treated hypertensive patients increases the risk of memory decline. Biennial neuropsychological evaluations were performed on 158 hypertensive subjects. Decline/year was measured on the Cued Selective Reminding test (total free recall and delayed recall) in three systolic BP groups (low-i.e., mean systolic BP during the follow-up period < 135 mm Hg; intermediate-i.e., 135 mm Hg < or = mean systolic BP < or = 150 mm Hg; high-i.e., mean systolic BP > 150 mm Hg). In total free recall, the three systolic BP groups had significantly different declines per year (P = .02), with patients in the high subgroup showing the greatest decline. In delayed recall, the three systolic BP groups also showed significantly different declines per year (P = .04), with patients in the low subgroup having the greatest decline. Chronically elevated systolic BP > 150 mm Hg is associated with accelerated memory decline compared to older treated hypertensive patients with systolic BP in an intermediate range. Chronically maintained systolic BP within a low normal range < 135 mm Hg in older treated hypertensive subjects may be associated with accelerated memory decline, specifically in a test of delayed memory recall, compared to patients with systolic BP in an intermediate range. Optimal regulation of systolic BP may be a potential modifiable risk factor to prevent or minimize memory loss in older hypertensive patients.     

Management of resistant hypertension in patients with carotid stenosis: high prevalence of renovascular hypertension

INTRODUCTION: Patients with carotid stenosis are at high risk of vascular events and therefore require an optimal control of risk factors such as hypertension. As the treatment of hypertension differs according to the cause, we examined the prevalence of resistant hypertension, and the cause of hypertension, among patients with carotid stenosis followed closely in two randomized trials of carotid endarterectomy. OBJECTIVE: The purpose of this study was to determine the prevalence of resistant hypertension and of secondary hypertension among patients with carotid stenosis. METHODS: A chart review was performed of all patients from our center who participated in the North American Symptomatic Carotid Endarterectomy Trial or the Asymptomatic Carotid Artery Study to determine the prevalence of renovascular hypertension. RESULTS: Among 170 patients with carotid stenosis followed in these two trials, 145 (83.5%) were hypertensive (systolic >160 or diastolic >90 mm Hg); at least 24 (14.1% overall, 16.6% of hypertensives) had renovascular hypertension based on either nuclear medicine renography, renal angiography or both; among the 79 patients with resistant hypertension (mean arterial pressure >130 mm Hg despite treatment), 20 (25.3%) had renovascular hypertension. Adrenocortical hyperplasia was the underlying cause of hypertension in 12 (7.1% of cases, 8.3% of hypertensives, 8.8% of resistant hypertensives). Blood pressures were significantly higher for patients with renovascular and adrenocortical hypertension (p < 0.0001 for systolic, p = 0.024 for diastolic pressures). CONCLUSION: Among patients with carotid stenosis, renovascular hypertension is unusually common. Resistant hypertension among such patients should lead to investigation and management directed at the cause of hypertension. Appropriate investigations might include plasma renin/aldosterone ratio, captopril renography and MRA of the renal arteries or renal angiography.     

Cerebroventricular dilation in spontaneously hypertensive rats (SHRs) is not attenuated by reduction of blood pressure

In previous studies, we found that spontaneously hypertensive rats (Okamoto-Aoki SHRs) suffer progressive postnatal dilation of the brain ventricles. In the present study we examined intracerebroventricular pressure and blood pressure as possible mechanisms of ventricular dilation in SHRs. We found that intracerebroventricular pressure was not elevated in SHRs. The role of blood pressure was examined in SHRs treated chronically with the antihypertensive drug, captopril, beginning in utero, and in renal hypertensive Sprague-Dawley rats (SDs). Although our experimental treatments produced significant changes in mean arterial pressures, they did not alter brain ventricular size: SDs with experimental hypertension had normal-sized brain ventricles and SHRs with pharmacologically reduced blood pressure had enlarged ventricles. These results suggest that neither increased intraventricular pressure nor high blood pressure is the sole cause of hydrocephalus in SHRs.     

Regional cerebral blood flow in conscious stroke-prone spontaneously hypertensive rats

Regional cerebral blood flow (rCBF) was measured autoradiographically with [14C]iodoantipyrine as a diffusible tracer in two strains of conscious normotensive rats (Wistar Kyoto and local Wistar) and in two groups of spontaneously hypertensive stroke-prone rats (SHRSP) with a mean arterial pressure (MAP) below or above 200 mm Hg. In spite of the large differences in arterial pressure, rCBF did not differ significantly between the hypertensive and the normotensive groups in any of the 14 specified brain structures measured. However, rCBF increased asymmetrically within part of the caudate-putamen in two of nine SHRSP with a MAP above 200 mm Hg, indicating a regional drop in the elevated cerebrovascular resistance.