Acute Blood Pressure Reduction Research Articles

The safety of adding carvedilol to hypertensive patients inadequately treated with diuretics

A single-blind, single-center study was conducted to investigate the short-term safety and efficacy of carvedilol, a new cardiovascular agent, when added to 25 mg hydrochlorothiazide (HCTZ) as combination therapy for patients inadequately treated with HCTZ alone. A total of 18 patients entered the baseline study phase, during which they received 25 mg HCTZ once daily for 4 weeks; 16 of these patients (8 men and 8 women) entered the combination treatment phase. All patients had a supine diastolic blood pressure (DBP) of greater than or equal to 95 mm Hg prior to receiving the first dose of combination treatment. Combination treatment consisted of 25 mg HCTZ plus 12.5 mg carvedilol once daily for 2 days, followed by a forced titration of the carvedilol dose to 25 mg for 7 days. After 2 days of 12.5 mg carvedilol plus 25 mg HCTZ once daily, mean trough blood pressure was reduced as compared with baseline values. Of 16 patients, 6 (38%) achieved a trough supine DBP of less than 90 mm Hg. After 1 additional week of combination therapy with 25 mg carvedilol, 8 of 15 patients (53%) achieved a trough supine DBP of less than 90 mm Hg and 14 of 15 patients (93%) achieved that of less than 95 mm Hg. At each visit during the combination treatment phase, the acute reduction in blood pressure was greatest during the first 2 h after dosing. The heart rate was minimally affected by combination treatment with carvedilol at either trough levels or acutely after dosing. Nine patients experienced adverse events during combination treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Reduction of Blood Pressure in Asymptomatic Patients With Severe Hypertension

Hypertension is a chronic disease. Except in cases of malignant hypertension or extremely rapid increases in arterial pressure, the end-organ damage due to hypertension develops over a period of years. Long-term treatment is usually necessary before beneficial effects on morbidity and mortality can be demonstrated. While the benefit of acute reduction of blood pressure in patients with hypertensive crisis (severe hypertension associated with encephalopathy, papilledema, pulmonary edema, or acute renal failure) has been shown, no benefit from acute reduction of blood pressure in asymptomatic patients has been or is likely to be demonstrated. Acute reduction of moderately to severely elevated arterial pressure in asymptomatic patients is based on four assumptions: (1) that it is important to reduce blood pressure immediately; (2) that oral antihypertensive loading produces more rapid or improved control of blood pressure; (3) that initiation of maintenance therapy sustains the achieved reduction in blood pressure; and (4) that

Acute reduction of blood pressure in asymptomatic patients with severe hypertension. An idea whose time has come--and gone

Acute reduction of blood pressure in asymptomatic patients with severe hypertension. An idea whose time has come--and gone

Comparative Renal Effects of Intravenous Administration of Fenoldopam Mesylate and Sodium Nitroprusside in Patients With Severe Hypertension

We studied the renal effects of intravenous administration of fenoldopam mesylate, a dopamine-1 agonist, vs sodium nitroprusside following acute reduction of blood pressure (BP) in 11 patients with severe hypertension (supine BP, 168/124 to 252/135 mm Hg). Following randomization (open-label), timed urinary and plasma samples for clearance of urea and creatinine and excretion of sodium, potassium, and calcium were obtained as well as plasma renin activity for a two-hour collection prior to infusion, during a two-hour period of BP control (supine diastolic BP, 95 to 110 mm Hg), and following two hours off the drugs. Mean arterial pressure was lowered similarly with the two drugs (-22% on fenoldopam vs -20% on nitroprusside; P = NS), and neither plasma renin activity nor plasma aldosterone concentration were changed by either drug. However, patients receiving fenoldopam had significant increases in urinary flow and excretion of sodium, potassium, and calcium, whereas patients receiving nitroprusside had no changes in these parameters. Patients receiving fenoldopam had a net fluid balance of -334 mL from the end of baseline to the end of the treatment period, while the nitroprusside group had a positive balance of 382 mL. Thus, these findings show that acute BP reduction with fenoldopam is associated with both a diuresis and natriuresis in severely hypertensive patients while lowering BP with nitroprusside does not predictably alter renal function and causes a moderate expansion in volume.

The influence of cilazapril on indices of autonomic function in normotensives and hypertensives.

1. In two single dose studies, acute blood pressure reduction with cilazapril was not associated with any significant change in supine or erect heart rate in either normotensives or hypertensives. 2. To investigate the lack of reflex cardioacceleration, a series of autonomic function tests was undertaken when there was maximum ACE inhibition, maximum evidence of angiotensin II withdrawal and the lowest blood pressure. 3. There was no evidence that cilazapril had any significant impact on indices of sympathetic nervous activity or the integrity of baroreflex mechanisms. 4. The results for the bradycardic response to apnoeic facial immersion, suggested enhanced parasympathetic activity, consistent with the withdrawal of the vagolytic actions of angiotensin II. 5. These results suggest that the absence of a heart rate response to ACE inhibition is not related to a profound sympatho-inhibitory effect or an impairment of baroreflex function. While there is some evidence of enhanced cardiac parasympathetic tone it seems unlikely that this is the sole explanation for the lack of cardioacceleration.

Comparative acute blood pressure reduction from intravenous fenoldopam mesylate versus sodium nitroprusside in severe systemic hypertension

Fenoldopam mesylate (SK&F 82526J) (FNP) is a specific postsynaptic dopamine-1 receptor agonist, 1 with weak α 2-antagonistic properties. 2 The agent is devoid of dopamine-2, α-1 or β-adrenergic activity. 3 Fenoldopam functions as an arteriolar vasodilator with dilation in the renal, mesenteric, skeletal muscle and lumbar beds. 4,5 Although a primary effect is through renal vasodilation with consequent increases in renal blood flow, 1–2,4–6 reduction in total peripheral resistance appears to be the mechanism of blood pressure (BP) reduction. 7,8 Furthermore, fenoldopam improves renal blood flow, fractional sodium and free water clearance while lowering BP. 4,9,10 Fenoldopam has a rapid onset (4 minutes) and a short duration of action (<10 minutes) with intravenous administration, 11 and has been reported to be an effective parenteral agent in severely hypertensive patients. 9 The agent undergoes sulfate, methylate and glucuronide conjugation, and produces no accumulation of toxic metabolic or degradation products. 12 Sodium nitroprusside (sodium nitroferricyanide) (NTP) has potent venodilating and arteriolar-dilating properties 13 and in many respects is an ideal antihypertensive agent when rapid reduction of BP is required. NTP quickly and reliably reduces BP in most patients and its short half-life aids in rapid titration of the drug. One major drawback associated with the use of NTP is that the very potency that gives it utility has often led to restrictions on its use. Restrictions include invasive monitoring requirements or use in an intensive care setting, thus dramatically escalating the cost associated with NTP's use. 14 A second drawback is that the formation of thiocyanate degradation products resulting in toxicity has limited its utility. 14 While thiocyanate toxicity has been primarily associated with impaired renal or hepatic function, in which the typical 4-day half-life of thiocyanate is prolonged, reports of toxicity in patients with normal renal function have also occurred. 14 Herein, we compared and evaluated the effects of sodium nitroprusside and intravenous fenoldopam mesylate in an open-label, randomized, multicenter trial of patients with severe systemic hypertension.

Nicorandil, a new vasodilator drug, in patients with essential hypertension

In 12 mild to moderate hypertensive patients we investigated the acute antihypertensive efficacy of three different doses of nicorandil, a new vasodilating agent which probably acts by increasing the potassium efflux from smooth muscle cells and causing a cellular hyperpolarization. After a 3-day placebo period the patients were given, according to a double-blind Latin-square randomized design, 10, 20 and 30 mg nicorandil as a single acute dose every other day. Blood pressure and the heart rate were measured in both supine and upright positions at various times for 24 h after the dosing; fractional urine collections were obtained at the end of the placebo period and after each active dose. All doses of nicorandil similarly and significantly (P less than 0.01) reduced supine blood pressure, with a peak after 4-6 h (10 mg: -21/-8 mmHg; 20 mg: -20/-9 mmHg; 30 mg: -29/-17 mmHg), and the effect was still present, though reduced, after 24 h; no change in the heart rate was observed. The results from the upright position were similar. There were no significant changes in urine volume and electrolyte excretion during the nicorandil administration. The three different doses of nicorandil caused similar acute blood pressure reductions without change in the heart rate, nor in the urine volume and urinary sodium.

The role of antihypertensive drugs in counteracting adverse influence on large arteries

Studies in humans have shown that chronic elevation of blood pressure induces early alterations in the large arteries, consisting mainly of increased diameter, increased pulse wave velocity, and decreased arterial compliance. Acute reduction of blood pressure, per se, does not necessarily correct these alterations homogeneously. For instance, cadralazine reduced brachial artery diameter and urapidil decreased pulse wave velocity, without accompanying changes in forearm arterial compliance. In contrast, acebutolol, isosorbide dinitrate, nicardipine, and nitrendipine, for the same acute decrease in blood pressure, improved forearm arterial compliance by a concomitant decrease in pulse wave velocity and increase in arterial diameter. To determine whether or not these vascular effects persist with long-term acebutolol therapy, nine hypertensive patients were treated for a period of 3 months. Forearm hemodynamic and cytosolic free calcium concentrations in platelets were simultaneously assessed before and after treatment. Compared with placebo baseline values, chronic acebutolol therapy significantly decreased mean arterial pressure ( p < 0.01), pulse wave velocity ( p < 0.01), and platelet free calcium concentration ( p < 0.05); forearm arterial compliance was increased ( p < 0.01), but brachial artery diameter did not change. Platelet calcium concentration correlated closely with pulse wave velocity even at constant mean arterial pressure. These findings suggest a relaxant effect of acebutolol on the smooth musculature of large arteries, which is independent of changes in blood pressure and arterial diameter, and possibly mediated by changes in cytosolic calcium levels.

Effects of acute reduction in blood pressure on the renal function of rats with diseased kidneys.

We studied the effect of an acute reduction in blood pressure, induced by diltiazem, on the renal hemodynamics of spontaneously hypertensive rats (SHR) with focal glomerular sclerosis, as induced by adriamycin (ADR). Renal plasma flow (RPF) and glomerular filtration rate (GRF) were determined before (first period) and during (second period) intravenous infusion of diltiazem in SHR 4-6 weeks after ADR treatment (group 1), 14-20 weeks after treatment (group 2), and in controls without treatment (group 3). Rats in group 1 had a normal renal function (RPF and GFR) in the first period, which was not significantly different from control rats (group 3). Rats in group 2 showed a reduced renal function, reflected by the lower levels of RPF and GFR, compared with groups 1 and 3. Mean blood pressure decreased equally in the 3 groups by about 50 mm Hg after the infusion of diltiazem. During the second period, 13.4 or 12.4% increase in RPF and a 29.0 or 23.2% elevation of GFR were evident in groups 1 or 3, respectively. In contrast, a 32.0% reduction of RPF was observed in group 2, accompanied by a 25.7% decline of GFR. A reduction in renal function (percent change of RPF or GFR) significantly correlated with the severity of renal dysfunction (RPF or GFR in the first period) in group 2. Thus, the renal function of rats with diseased kidneys is sensitive to an acute reduction in blood pressure by diltiazem, and the sensitivity depends on the degree of renal deterioration.

Hypertensive emergencies.

Hypertensive emergencies are defined as conditions where a seriously elevated blood pressure imposes a substantial threat to a patient's life or vital organ functions. Since acute blood pressure reduction by lowering cardiac output and/or vascular resistance itself has the potential for serious and even life-threatening complications, treatment should be given restrictively based on pathophysiological considerations concerning altered patterns of blood pressure and blood flow regulation in these patients. Ischemic treatment related complications can be avoided by a rational choice of first-line drugs. These include beta-blockers for patients with a compromised myocardial oxygen supply as in acute myocardial infarction and unstable angina as well as for patients with dissecting aneurysms and patients with pronounced catecholamine release. In other types of hypertensive emergencies, calcium antagonists have emerged as the treatment of choice with excellent efficacy and a favorable risk-benefit ratio. Sodium nitroprusside is rarely necessary in treatment failures after calcium channel blockade.

Baroreflex Control of Heart Rate and Renin Release in SHR Following Administration of Felodipine, an Antihypertensive Ca2+ Antagonist

Baroreflex control of renin release following acute and prolonged blood pressure reduction by felodipine administration was investigated in conscious spontaneously hypertensive rats (SHR) fitted with arterial and venous catheters. Basal values of mean arterial pressure (MAP), heart rate (HR), and plasma renin activity (PRA) were obtained in SHR and in SHR given felodipine for 2 weeks (SHRF). In SHRFMAP was reduced by 12% (p less than 0.01) versus SHR, but PRA and HR were similar. Acute i.v. infusion of felodipine, during 5 h, maintained MAP reduction by 40%. Initially, HR increased 29 +/- 3% but returned to predrug levels after 3 h. PRA increased from 1.4 +/- 0.5 to 6.5 +/- 1.0 ng/ml/h. After 5 h PRA had reached low levels equal to those in SHR given placebo instead of felodipine. In SHR pretreated with metoprolol neither HR nor PRA increased following felodipine, an indication that the observed changes were neurogenically determined. This suggests that baroreflex control of cardiac and renal function resets within 3-5 h following blood pressure reduction by felodipine.

Acute effect of nifedipine on blood pressure and left ventricular ejection fraction in severely hypertensive outpatients: Predictive effects of acute therapy and prolonged efficacy when added to existing therapy

Nifedipine is known to reduce blood pressure both acutely and chronically. However, the following questions remain to be answered: (1) can nifedipine be given acutely and safety to patients with severe hypertension in an outpatient setting, (2) would its efficacy be retained with long-term therapy, and (3) is nifedipine safe in the presence of cardiomegaly? Nifedipine (10 mg capsule sublingually) was given to 46 outpatients with severe or apparently refractory hypertension; 19 were followed-up for 18 months and 18 for 24 months. Nifedipine reduced blood pressure acutely and safely in 43 of 46 outpatients (mean control diastolic pressure 137 mg Hg), irrespective of prior treatment regimen. Blood pressure levels after 2 to 24 months of twice daily oral nifedipine (10 mg) were similar to 20-minutes levels, showing that tolerance did not occur. In a separate series of 37 patients, who had radiologic cardiomegaly in addition to hypertension, the control ejection fraction was 62%. Nifedipine, when used acutely, slightly increased the ejection fraction to 65% ( p < 0.005). Our studies show that in outpatients with severe hypertension, sublingual nifedipine is an antihypertensive agent which acts swiftly and safely, without causing a decrease in the ejection fraction when it is used for acute blood pressure reduction, and that subsequent therapy with oral nifedipine results in a predictive long-term hypotensive effect.

Osmoregulation and Baroregulation of Plasma Vasopressin in Essential Hypertension

Vasopressin secretion is stimulated by hyperosmolality, hypovolemia, or hypotension and is inhibited by hypoosmolality, hypervolemia, or hypertension. These osmotic and hemodynamic influences are mediated by neuronal afferents that originate in separate osmoreceptors or baroreceptors but ultimately converge to act on the same neurosecretory neurons. Functionally, the two control systems are integrated in such a way that osmoregulation is altered but not disrupted by hemodynamic influences. In patients with uncomplicated essential hypertension, basal as well as osmotically stimulated vasopressin is completely normal. The vasopressin response to an acute reduction in blood pressure is also normal if the values are expressed relative to the change in pressure. However, if the plasma vasopressin response is plotted as a function of absolute blood pressure, the line describing the relationship lies well to the right of normal. Thus, although it is completely intact, the baroregulatory mechanism appears to be reset to a higher level in essential hypertension. These results suggest that increased secretion of vasopressin does not contribute to the genesis or maintenance of uncomplicated, untreated essential hypertension but may antagonize the therapeutic effect of some antihypertensive drugs. If so, antagonists of V1 receptors may be useful as second-line adjunctive therapy for this condition.

Treatment of hypertensive emergencies with the calcium channel blocker nifedipine

The severe elevations in blood pressure that occur in hypertensive emergencies pose a serious threat to life or vital organ functions. However, use of antihypertensive agents to acutely reduce blood pressure during hypertensive emergencies may cause deficits in the perfusion of the central nervous system or the heart. Therefore, a knowledge of cerebral blood flow regulation during acute treatment of hypertensive emergencies is indispensable. Experience with the calcium channel blocker nifedipine in the acute treatment of patients with hypertensive emergencies has shown that this agent has a pronounced vasodilatory effect, especially in vessels with a high vasoconstrictor tone, and that it does not reduce cardiac output or cerebral blood flow. The drug is highly efficacious and safe, and reports of serious side effects are rare. However, nifedipine should be used with caution in patients with suspected or proved critical arteriosclerotic stenosis of the cerebral arteries, because a reduction in perfusion pressure with any drug places these patients at risk for development of ischemic symptoms. Nifedipine can be used as a first-line drug for acute reduction of blood pressure in patients with hypertensive emergencies.

Transcutaneous oxygen tension (TcPO2) during nonnutritive sucking (NNS) in preterm infants

There is evidence of hypertensive effects caused by anabolic androgenic steroids (AAS). A single exercise session promotes the acute reduction of blood pressure, but the effects of AAS on this phenomenon are unknown.To investigate the post-exercise blood pressure response in androgenic-anabolic steroid users.Thirteen AAS users (23.9 ± 4.3 years old) and sixteen controls (22.1 ± 4.5 years old) performed a session of aerobic exercise. Heart rate and blood pressure were assessed before exercise and during a 60 min post-exercise resting period. Repeated ANOVA measures were used to determine differences between the groups.While the control group had a significant reduction in post-exercise systolic blood pressure of up to 13.9 ± 11.6 mmHg at 40 min, this phenomenon was limited among AAS users who reached a maximum of 6.2 ± 11.5 mmHg at 60 min. The between groups comparison revealed significant higher post-exercise hypotension (PEH) for the control group at 30 min (−12.9 ± 14.1 mmHg versus −2.9 ± 7.6 mmHg), 40 min (−13.9 ± 11.6 mmHg versus −2.5 ± 8.3 mmHg), 50 min (−13.9 ± 13.9 mmHg versus −5.0 ± 7.9 mmHg) and 60 min (−12.5 ± 12.8 mmHg versus −6.2 ± 11.5 mmHg). There was no significant diastolic PEH in any of the groups.This study demonstrated impaired systolic post-exercise hypotension as a new adverse effect of AAS usage.

Effects of reduced renal artery pressure on feedback control of glomerular filtration.

ARTICLESEffects of reduced renal artery pressure on feedback control of glomerular filtrationG. Selen, and A. E. PerssonG. Selen, and A. E. PerssonPublished Online:01 Mar 1983https://doi.org/10.1152/ajprenal.1983.244.3.F342MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByHigh salt exacerbates acute kidney injury by disturbing the activation of CD5L/apoptosis inhibitor of macrophage (AIM) protein29 November 2021 | PLOS ONE, Vol. 16, No. 11“I don’t get no respect”: the role of chloride in acute kidney injuryJoshua L. Rein and Steven G. Coca14 March 2019 | American Journal of Physiology-Renal Physiology, Vol. 316, No. 3Renal Autoregulation in Health and DiseaseMattias Carlström, Christopher S. Wilcox, and William J. Arendshorst1 April 2015 | Physiological Reviews, Vol. 95, No. 2Assessment of renal autoregulationWilliam A. Cupples, and Branko Braam1 April 2007 | American Journal of Physiology-Renal Physiology, Vol. 292, No. 4Mechanisms of renal blood flow autoregulation: dynamics and contributionsArmin Just1 January 2007 | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, Vol. 292, No. 1ANG II-induced downregulation of RBF after a prolonged reduction of renal perfusion pressure is due to pre- and postglomerular constrictionCharlotte Mehlin Sorensen, Paul Peter Leyssac, Max Salomonsson, Ole Skott, and Niels-Henrik Holstein-Rathlou1 May 2004 | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, Vol. 286, No. 5Resetting of renal blood autoregulation during acute blood pressure reduction in hypertensive ratsBjarne M. Iversen, Fred Ivan Kvam, Knut Matre, and Jarle Ofstad1 August 1998 | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, Vol. 275, No. 2 More from this issue > Volume 244Issue 3March 1983Pages F342-F348 Copyright & PermissionsCopyright © 1983 the American Physiological Societyhttps://doi.org/10.1152/ajprenal.1983.244.3.F342PubMed6829766History Published online 1 March 1983 Published in print 1 March 1983 Metrics

Altered blood pressure and renin responses to converting enzyme inhibition after aprotinin-induced kallikrein-kinin-system blockade.

1. The effect of aprotinin-induced blockade of the kallikrein-kinin system on haemodynamic and biochemical responses to converting enzyme inhibition by SQ 14 225 was evaluated in 26 patients with essential hypertension. 2. SQ 14 225 lowered blood pressure in high, normal and low renin hypertension. In low and normal renin patients, but not in high renin patients, the acute blood pressure-lowering effect of SQ 14225 could be overcome by aprotinin. Aprotinin infusion produced small vasopressor effects in all groups of patients. 3. Aprotinin lowered the level of circulating active renin but not that of inactive renin. 4. It is concluded that in low and normal, but not in high, renin hypertensive patients activation of the kallikrein-kinin system is responsible for the acute blood pressure reduction observed with converting enzyme inhibitions. 3. Aprotinin lowered the level of circulating active renin but not that of inactive renin. 4. It is concluded that in low and normal, but not in high, renin hypertensive patients activation of the kallikrein-kinin system is responsible for the acute blood pressure reduction observed with converting enzyme inhibition. 5. With long-term converting enzyme inhibition kallikrein-kinin system activation seems to play only a minor role. 6. The kallikrein-kinin system may be involved in the regulation of blood pressure. 7. There is no direct evidence of a participation of kallikrein in the activation of prorenin in vivo.

Effects of blood pressure manipulations on shivering thermogenesis in the pigeon

The effects of blood pressure (BP) manipulations on shivering thermogenesis were studied in conscious pigeons. A rise in BP induced by noradrenaline (NA) or equipotent doses of angiotensin II (Ang II) effectively suppressed shivering at +12 degree C and partly abolished the cold-induced vasoconstriction in the feet. The inhibition commenced when the rise in BP reached +40 mmHg, and a fall in body temperature followed these responses. Comparison of the trajectories in the BP-shivering plane revealed that the inhibition of shivering by Ang II could be completely explained by changes in BP, whereas NA had also another, more prolonged inhibitory action independent of baroreceptor activity. A similar dose-dependence for effects on BP and shivering could be established with both drugs. An acute reduction of BP by sodium nitroprusside had also a very potent inhibitory effect on shivering. In hypotensive pigeons elevation of BP with NA initially enhanced shivering, but when BP was raised beyond normal levels shivering was again suppressed. We conclude that both a rise and a fall in BP can inhibit shivering in the pigeon, and that normal levels of BP facilitate shivering. NA inhibits shivering by more than one mechanism, but the initial effect is mediated through a baroreflexive action. The interactions of thermoregulatory and cardiovascular mechanisms suggest an integrated control of body temperature and circulation, which should be considered in experimental approaches to these homeostatic systems.

The effect of prostaglandin synthesis inhibition of the acute blood pressure reduction by captopril in pentobarbital-anaesthetized rats

Treatment of pentobarbital-anaesthetized rats with captopril (SQ 14225) caused a reduction in mean arterial blood pressure (MAP), which lasted for over 1 h when a dose of 5 mg/kg i.p. was used. Pretreatment with the prostaglandin synthesis inhibitors indometacin (IND, 5 mg/kg i.p.) or acetylsalicylic acid (ASA, 100 mg/kg i.p.) did not prevent the initial decrease in MAP after captopril. However, the recovery of the MAP was much faster than after captopril alone. In rats pretreated with IND, the MAP after captopril was significantly higher than after captopril alone from 30 min onwards. With ASA pretreatment the same was observed after 45 min. These data indicate that the subacute blood pressure lowering effect of captopril in pentobarbital-anaesthetized normotensive rats may be at least partly dependent on the presence of an intact prostaglandin biosynthetic pathway. This may be due to activation of prostaglandin synthesis by the accumulation of bradykinin and angiotensin I after captopril.

Effects of blood pressure reduction on the structural vascular abnormality in skin and muscle vascular beds in human essential hypertension.

1. Vascular resistance at maximal vasodilatation was examined in two vascular beds in two groups of hypertensive patients and in normotensive control subjects before and during anti-hypertensive therapy in the hypertension groups. 2. In one group of twelve untreated patients with essential hypertension, examined with plethysmography and intra-arterial blood pressure recording, a significantly higher vascular resistance at maximal vasodilatation was found in the hands compared with normotensive control subjects matched for age, sex, weight and height. This indicated a structural vascular abnormality in the patient group. 3. After 5 years of anti-hypertensive therapy in the patient group the difference in vascular resistance between patients and control subjects had decreased significantly, indicating a reversibility of the structural vascular abnormality. 4. Vascular resistance at maximal vasodilatation was examined in the calves of twelve untreated patients with essential hypertension and fourteen normotensive control subjects. Plethysmographic technique and indirect blood pressure recordings were used. A significantly higher vascular resistance was found in patients than in control subjects, indicating a structural vascular abnormality also in this vascular bed. 5. Anti-hypertensive treatment for 6 months in the patient group did not change vascular resistance at maximal dilatation, indicating that the structural vascular abnormality remained. 6. During acute reduction of blood pressure in hypertension by means of trimethaphan infusion, blood pressure and blood flow to the hands were reduced proportionally with no change of vascular resistance at maximal vasodilatation. 7. This indicates that resistance at maximal dilatation was unaffected by the acute reduction of blood pressure, in contrast to the findings after prolonged reduction of blood pressure in this vascular bed.