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PubMed1992

Chronic lesion of rostral ventrolateral medulla in spontaneously hypertensive rats.

We studied the effects of chronic selective neuronal lesion of rostral ventrolateral medulla on mean arterial pressure, heart rate, and neurogenic tone in conscious, unrestrained spontaneously hypertensive rats. The lesions were placed via bilateral microinjections of 30 nmol/200 nl N-methyl-D-aspartic acid. The restimulation of this area with N-methyl-D-aspartic acid 15 days postlesion failed to produce a pressor response. One day postlesion, the resting mean arterial pressure was significantly decreased in lesioned rats when compared with sham rats (100 +/- 7 versus 173 +/- 4 mm Hg, p less than 0.05). Fifteen days later, the lesioned group still showed values significantly lower than the sham group (150 +/- 6 versus 167 +/- 5 mm Hg, p less than 0.05). No significant heart rate differences were observed between the sham and lesioned groups. The ganglionic blocker trimethaphan (5 mg/kg i.v.) caused similar reductions in mean arterial pressure in both lesioned and sham groups. The trimethaphan-induced hypotension was accompanied by a significant bradycardia in lesioned rats (-32 +/- 13 beats per minute) but a tachycardia in sham rats (+33 +/- 12 beats per minute) 1 day postlesion. Therefore, rostral ventrolateral medulla neurons appear to play a significant role in maintaining hypertension in conscious spontaneously hypertensive rats. Spinal or suprabulbar structures could be responsible for the gradual recovery of the hypertension in the lesioned rats.

Animals↗
PubMedDate not supplied

Pyramidal tract responses (PTR) during hypoxia and hypotension.

In rats with unilateral carotid artery ligation pyramidal tract responses were studied during hypoxia and during trimethaphan-induced hypotension. Observations on EEG activity during hypoxia suggest that unilateral carotid artery ligation produces a more severe perfusion defect in lateral portions of the hemisphere. During hypoxia and during trimethaphan-induced hypotension indirect PTRs disappeared first from the hemisphere on the side of carotid artery ligation and next from the opposite hemisphere. This was followed by loss of direct PTRs in the same order. Animals could not be resuscitated once the direct PTR from the non-ligated hemisphere had disappeared. Hypotension appears to be a late contributing factor in impairing electrocerebral activity during hypoxia in this study.

Animals↗
PubMed1976

The effect of changes in perfusion pressure on uteroplacental blood flow in the pregnant rabbit.

The effect of perfusion pressure on uteroplacental blood flow was determined in pregnant rabbits utilizing the radioactive microsphere method. Control mean arterial pressure, 93 mm Hg +/- 2.6 SEM, was raised by carotid ligation to 109 +/- 4.1 mm Hg and then reduced with antihypertensive drugs to 74 +/- 1.3 mm Hg. Over this range of pressure there was no significant change in cardiac output, 605 +/- 36, 523 +/- 37, and 540 +/- 39 ml/min; or uteroplacental blood flow, 30 +/- 3.2, 27 +/- 5.2, and 29 +/- 4.5 ml/min, respectively. When prostaglandin synthesis was inhibited with either indomethacin or meclofenamate (2 mg/kg), uterine vascular resistance was higher but maintenance of uteroplacental flow occurred over a perfusion pressure of 89 +/- 6.7-115 +/- 9.3 mm Hg. With more severe hypotension induced with trimethaphan, control arterial pressure fell from 92 +/- 2.4 to 39 +/- 0.9 mm Hg, cardiac output fell from 514 +/- 17 to 407 +/- 22 ml/min (P less than 0.025) and uteroplacental blood flow fell from 6.1 +/- 0.9 to 2.5 +/- 0.9% of cardiac output (P less than 0.05), which represented an absolute fall from 32.4 +/- 5 to 10.6 +/- 3 ml/min (P less than 0.025). There was no significant change in renal blood flow expressed as percentage of cardiac output, 14.9 +/- 2 and 13 +/- 1.5%, or in absolute flow, 75 +/- 7.7 and 54 +/- 7 ml/min with trimethaphan-induced hypotension. These studies indicate that uteroplacental blood flow is maintained relatively constant over a range of perfusion pressure of 60-140 mm Hg in both normal and prostaglandin-inhibited pregnant rabbits. However, with reduction in pressure to 36-42 mm Hg, uteroplacental blood flow falls, expressed as a percentage of cardiac output and in absolute flow.

Animals↗
PubMed1993

Blood Pressure, Memory, and Electroconvulsive Therapy.

Blood pressure changes recorded during electroconvulsive therapy (ECT) in 23 psychiatric in-patients with major depressive disorders correlated with and predicted the degree of anterograde memory changes measured 48-72 h after ECT. The Randt memory test was the principal measure of memory change. A subgroup of older patients with cardiovascular illness received trimethaphan, a ganglionic blocker that impedes a hypertensive surge during the treatment. They did not differ in memory function from a younger subgroup that did not receive trimethaphan. Control of the hypertensive response in the older age group counterbalanced the additional memory dysfunction that was anticipated as a result of advanced age and cardiovascular pathology.

Journal Article↗
PubMed1995

Hypertensive emergencies.

Hypertensive emergencies are uncommon and physiologically diverse. Consequently, it is difficult for most physicians to develop a familiarity with all the different hypertensive crises and with all drugs available for treating them (Table 4). Clinicians should not agonize over which is the perfect therapeutic agent for a particular emergency, but instead, they should focus on scrupulous monitoring and familiarize themselves with a few agents that will serve in most situations. Generally, these agents will be sodium nitroprusside and nitroglycerin. Vigilant neurologic monitoring is mandatory in all hypertensive emergencies. The early symptoms and signs of cerebral hypoperfusion can be vague and subtle, but if recognized, serious complications of therapy can be avoided. Remember, the patient may still be hypertensive. Avoid acute (during the first hour) reductions in MAP of more than 20% whenever possible; subsequent reductions should be gradual. In patients known to have markedly elevated ICP and who need acute reductions in their BP, serious consideration should be given to direct monitoring of the ICP so that CPP can be maintained within safe limits. In general, oral agents should not be used for the treatment of hypertensive emergencies. Intravenous Labetalol and intravenous nicardipine are not suitable for general use in hypertensive emergencies. In special situations (e.g., perioperative hypertension and subarachnoid hemorrhage), however, they may be employed. Their role may expand with further study. Trimethaphan may be superior to nitroprusside for hypertension complicated by elevated ICP or cerebral dysfunction. Realistically, most physicians will continue to use nitroprusside. Intense neurologic monitoring is more important than the specific agent used. Nitroglycerin is the agent of choice for acute ischemic heart disease complicated by severe hypertension; if it fails, use nitroprusside. For aortic dissection, the combination of nitroprusside and IV propranolol is the therapy of choice; beta-blockade must be achieved rapidly or the dissection may worsen. Trimethaphan is also an agent for first-line therapy. Esmolol is an alternative to IV propranolol for the treatment of aortic dissection, if prolonged beta-blockade might seriously jeopardize the patient. For eclampsia, unless an expert in hypertension during pregnancy has established an alternative, the therapy of choice is hydralazine and magnesium. The treatment of subarachnoid hemorrhage is in flux; calcium channel blockers are used to prevent spasm, not to lower BP. If the BP must be lowered immediately, use nitroprusside.

Antihypertensive Agents↗
PubMed1996

The membrane hyperpolarization of rat dorsolateral septal nucleus neurons is mediated by a novel nicotinic receptor.

The pharmacology, calcium dependence and G protein mediation of the membrane hyperpolarization of rat dorsolateral septal nucleus (DLSN) neurons in response to nicotinic agonists was examined to classify the nicotinic receptor mediating the response. Intracellular recording from DSLN neurons in a brain slice preparation was used to determine whether chlorisondamine, trimethaphan, cytisine or strychnine inhibited the membrane hyperpolarization in response to application of the nicotinic agonist 1,1-dimethyl-4-phenylpiperazinium (DMPP). Chlorisondamine was found to block the response only at a high concentration (500 microM) although strychnine (100 microM) was without effect. Cytisine was neither an effective agonist nor an antagonist (500 microM). Surprisingly, trimethaphan appeared to act as an agonist, rather than an antagonist, with a potency and efficacy similar to that reported for nicotine at this receptor. The response was dependent on intracellular calcium stores because it persisted in the absence of extracellular calcium but was blocked by intracellular injection of 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA). Injection of GTP gamma S into the neurons blocked the nicotinic response. Apamin, iberiotoxin and charybdotoxin reduced but did not block the response at concentrations that selectively block calcium-dependent potassium channels. These results indicate that the nicotinic response in DLSN neurons may be mediated by a metabotropic nicotinic receptor coupled to a calcium-dependent potassium channel through the activation of a G-protein and release of intracellular calcium stores. The unusual pharmacology of the nicotinic receptor on DLSN neurons indicates that it may be a novel receptor which has yet to be cloned.

Animals↗
PubMed1975

Effects of hypotension on rhesus monkeys.

Twenty-one late-juvenile rhesus monkeys were rendered profoundly hypotensive for 0-, 15-, or 30-minute periods by means of infusion of trimethaphan camsylate. Blood pressure was then restored to prehypotensive levels with phenylephrine infusions. Respiratory gas tensions and pH of arterial blood were maintained within their normal limits throughout experimental and recovery periods. Animals either recovered and showed no sequelae or diet 12 to 48 hours later of cardiorespiratory difficulties, often accompanied by brain swelling. Brain injury and death occurred in 64% of cases when arterial blood pressure was maintained at 25 mm Hg for up to 30 minutes. Multifocal myoclonus, depressed electroencephalographic activity, rises in cisternal cerebrospinal (CSF) pressure, respiratory depression, and characteristic changes in serum and cisternal CSF glucose followed episodes of controlled hypotension. Hypoxia and acidosis occurring during insult or recovery periods rather than hypotension itself probably account for neuropathological sequelae described by others.

Animals↗
PubMed1997

6-[18F]fluorodopamine positron emission tomographic scanning in the assessment of cardiac sympathoneural function--studies in normal humans.

Thoracic positron emission tomographic (PET) scanning after injection of 6-[18F]fluorodopamine ([18F]-6F-DA) visualizes cardiac sympathetic innervation. We tested whether changes in curves relating myocardial [18F]-6F-DA-derived radioactivity with time (time-activity curves, TACs) can reflect changes in important aspects of cardiac sympathetic function. Thoracic PET scans were obtained after intravenous administration of [18F]-6F-DA or the perfusion imaging agent [13N]ammonia into normal volunteers. Ganglion blockade with trimethaphan (TRI) was used to decrease sympathoneural traffic, desipramine (DMI) to block neuronal uptake of catecholamines, and tyramine (TYR) to displace vesicular amines. After [18F]-6F-DA administration, myocardial concentrations of [18F]-6F-DA-derived radioactivity declined bi-exponentially from the peak value. TRI increased the y-intercept (yo) value for the early phase (p = 0.01), and DMI decreased the yo for the late phase (p = 0.01). The TRI effect did not result from increased arterial [18F]-6F-DA concentrations or from increased myocardial perfusion. TYR infusion, begun 90 min after [18F]-6F-DA administration, accelerated the decline of myocardial radioactivity by 2.6-fold (p = 0.003). Alterations in post-ganglionic sympathoneural traffic, neuronal catecholamine uptake, and vesicular turnover of monoamines produce distinct changes in myocardial TACs after [18F]-6F-DA injection. [18F]-6F-DA PET scanning may therefore enable assessments of effects of stressors, drugs, and neurocardiological disorders on specific aspects of cardiac sympathoneural function.

Adrenergic Uptake Inhibitors↗
PubMed1998

Hyper-responsiveness of adrenal sympathetic nerve activity in spontaneously hypertensive rats to ganglionic blockade, mental stress and neuronglucopenia.

Previous investigations indicate that the spontaneously hypertensive rat (SHR) has elevated sympathetic tone at rest. The present study aimed to determine whether SHR has exaggerated sympatho-adrenal activation in response to various sympathetic stimuli. The mean blood pressure (MBP), heart rate (HR) and preganglionic adrenal sympathetic nerve activity (SNA) were recorded from conscious, unrestrained SHR and from its normotensive control, the Wistar-Kyoto rat (WKY) (n=7, respectively).Ganglionic blockade (trimethaphan, 5 mg/kg) reduced MBP identically in both groups of rats. It did not change HR in SHR, but increased HR significantly in WKY (P<0.05). The adrenal SNA increased in both groups, but the magnitude of the increase was more than threefold greater in SHR (P<0.05). Mental stress caused by air-jet induced significantly greater tachycardia (threefold) and sympatho-adrenal activation (tenfold) in SHR than in WKY rats. In SHR the inhibition of glycolysis (2-deoxy-d-glucose, 500 mg/kg) also produced a profound activation of adrenal SNA (sevenfold) and the increased adrenal SNA was not paralleled by an increased HR. We conclude that a variety of sympathetic stimuli, including ganglionic blockade, mental stress and neuronglucopenia, cause exaggerated activation of preganglionic adrenal SNA in SHR compared with WKY, indicating that adrenal SNA in SHR is hyper-responsive.

Adrenal Glands↗
PubMed2006

Alternative to ganglionic blockade with anticholinergic and alpha-2 receptor agents.

The ganglionic blocking agent trimethaphan (TMP) is no longer produced. Therefore, a need exists for alternative pharmacological approaches to investigate baroreflex control of the circulation. The aim of the present study was to examine baroreflex-mediated cardiovascular responses during the administration of a muscarinic receptor antagonist (glycopyrrolate; GLY: ) and a selective alpha-2 receptor agonist (dexmedetomidine; DEX: ) and to compare responses to ganglionic blockade with TMP. We hypothesized that combined GLY-: DEX: would inhibit the baroreflex similar to TMP. Ten volunteers participated in two study days and were instrumented with pulse oximeter, nasal cannula, ECG, continuous blood pressure monitoring (Finapres), and I.V. catheter for drug infusions. Each study day consisted of a control condition followed by either combined GLY: -DEX: or TMP on alternating days. A Valsalva maneuver was performed under each condition with every subject and six subjects received bolus phenylephrine (25 mug) during GLY: -DEX: and TMP. Combined GLY: -DEX: increased (P < 0.05) blood pressure (99 +/- 4 mmHg) and heart rate (99 +/- 3 bpm) relative to control condition (BP: 90 +/- 2 mmHg; HR: 64 +/- 3 bpm) and TMP infusion decreased (P < 0.05) blood pressure (79 +/- 3 mmHg) while increasing heart rate (88 +/- 3 bpm). Valsalva maneuver elicited a persistent drop in arterial pressure (no phase IIb recovery) with the absence of a phase IV overshoot during both GLY: -DEX: and TMP conditions. Phenylephrine increased systolic pressure 34 +/- 4 mmHg under GLY: -DEX: and 23 +/- 3 mmHg with TMP (P < 0.05). Heart rate only decreased 1 +/- 2 bpm during GLY: -DEX: and 1 +/- 1 bpm with TMP. Taken together, our results suggest that GLY: -DEX: is a reasonable alternative to TMP for baroreflex inhibition.

Adrenergic alpha-2 Receptor Agonists↗
PubMed1994

Intracerebellar nicotinic-cholinergic participation in the cerebellar adenosinergic modulation of ethanol-induced motor incoordination in mice.

Many epidemiological studies have suggested a high correlation between the use of tobacco and ethanol, the two most frequently abused psychoactive drugs. Recently, we reported behavioral interactions between (-)-nicotine, (-)-cotinine and ethanol within the CNS. The present report is a confirmation and an extension of that study. Using a 2 g/kg ethanol-induced motor incoordination (EIMI) as the test response, possible behavioral interactions between (-)-nicotine, (-)-cotinine and ethanol and between (-)-nicotine, (-)-cotinine and adenosine agonist + ethanol in the cerebellum were investigated. (-)-Nicotine, 0.625, 1.25 and 5 ng intracerebellarly (ICB) significantly attenuated EIMI in a dose-related manner. Likewise, ICB injection of 1.25, 2.5, and 5 ng (-)-cotinine, a major metabolite of nicotine, significantly attenuated EIMI after the same i.p. dose of ethanol as in case of (-)-nicotine but less markedly compared to (-)-nicotine. No change in normal motor coordination was observed when the highest dose of (-)-nicotine or (-)-cotinine was injected ICB followed by saline control, suggesting selectivity of their behavioral interactions with ethanol. The attenuation of EIMI by (-)-nicotine and (-)-cotinine was blocked by ICB hexamethonium (1 microgram) and trimethaphan (100 ng), the purported nicotinic-cholinergic antagonists. Finally, the ICB injection of adenosine agonists, N6-cyclohexyladenosine (CHA) or 5'-N-ethylcarboxamidoadenosine (NECA), produced marked accentuation of EIMI which was significantly antagonized by ICB (-)-nicotine and (-)-cotinine. The data obtained in the present study suggested, for the first time, a cerebellar adenosinergic-nicotinic cholinergic interaction and modulation of EIMI. The data also suggested participation of cerebellar nicotinic-cholinergic receptors in EIMI.

Adenosine↗
PubMed1994

Striatal extracellular dopamine levels are not increased by hyperglycemic exacerbation of ischemic brain damage in rats.

We tested the hypothesis that hyperglycemic exacerbation of incomplete forebrain ischemia is mediated by increased extracellular dopamine levels. Normoglycemic and hyperglycemic Sprague-Dawley rats (eight each) with previously placed coaxial striatal microdialysis probes underwent 12 min of forebrain ischemia produced by bilateral carotid artery occlusion and trimethaphan-induced hypotension. Microdialysis was performed before, during, and for 6 h after ischemia, then perfusion-fixation was performed. Hyperglycemic rats had more severe postischemic damage in the caudate-putamen, neocortex, and hippocampus. Extracellular striatal dopamine levels were increased by ischemia, but were unaffected by hyperglycemia. These data show that hyperglycemic exacerbation of ischemic striatal damage does not depend on elevated extracellular dopamine levels.

Animals↗
PubMedDate not supplied

Diminished baroreceptor sensitivity in elderly hypertensives. Possible role of atherosclerosis.

Baroreceptor sensitivity was studied in twelve young normotensive subjects and forty hypertensive patients, separated into two groups according to their age, severity of hypertension and signs of severe atherosclerotic vascular disease. Under stabilized circulatory conditions, the changes of pulse rate in response to changes of blood pressure, attained by infusion of trimethaphan camphorsulfonate alone or with norepinephrine, was examined. There was gradually diminished change of pulse rate in relationship to blood pressure change as age and hypertension advanced. However, although the blood pressure threshold of stimulation was obviously higher in the middle-aged hypertensive subjects than in the normotensive ones, the slightly reduced baroreceptor sensitivity was not significantly different from that in the normotensive group. Only in the elderly hypertensive patients was significantly diminished baroreceptor sensitivity demonstrated, which was also significantly different from that in the middleaged hypertensive patients. It is speculated that the significantly diminished baroreceptor sensitivity found in the elderly hypertensive patients may be due to atherosclerotic changes in the region of the baroreceptor, although proof of that is not available at the present time.

Adult↗
PubMed1993

Central behavioral interactions between ethanol, (-)-nicotine, and (-)-cotinine in mice.

A high correlation between alcohol use and smoking has long been suggested by epidemiological data. We examined the potential behavioral interactions between ethanol and nicotine using ethanol-induced motor incoordination as the test response in mice. Effect of pretreatment of various doses of (-)-nicotine, (-)-cotinine, a major metabolite of nicotine, and (+)-nicotine administered ICV on ethanol (IP)-induced motor incoordination was investigated. (-)-Nicotine (0.19, 0.38, 0.77 and, 1.54 nmoles ICV) produced significant attenuation of motor incoordination due to ethanol (2 g/kg IP) in a nearly dose-related manner which was blocked by ICV hexamethonium and trimethaphan, both purported nicotinic antagonists. (-)-Cotinine (0.35, 0.70, 1.41 nmole ICV) produced similar attenuation but was les potent than (-)-nicotine. Attenuation by (+)-nicotine (0.19, 0.38, and 0.77 nmoles ICV) was also significant but only at 0.77 nmole dose level. (+)-Nicotine-induced attenuation of motor incoordination by ethanol was antagonized by nicotinic antagonists. Data obtained suggest a central behavioral interaction between ethanol and nicotine at least through the participation of cholinergic nicotinic receptors.

Alcoholic Intoxication↗
PubMed1998

Age, hypertension, and cardiac responses to beta-agonist in humans.

OBJECTIVES: To evaluate the effects of hypertension on heart rate and left ventricular responses to beta-agonist in young and older subjects, as well as the modulating effect of the arterial baroreflex on these responses. METHODS: Isoproterenol (INN, isoprenaline) alone was infused in 14 young normotensive subjects (mean age, 30 +/- 2 years), 18 older normotensive subjects (mean age, 60 +/- 2 years), 11 young hypertensive subjects (mean age, 36 +/- 1 years), and 17 older hypertensive subjects (mean age, 59 +/- 1 years); isoproterenol combined with ganglionic blockade (trimethaphan [INN, trimetaphan]) was administered to eight young normotensive subjects and eight young hypertensive subjects. Isoproterenol was infused at three to four incremental rates, each rate for 8 minutes. Left ventricular responses were assessed by echocardiography. RESULTS: Isoproterenol caused similar increases in heart rate in all four groups. With ganglionic blockade, heart rate responses were enhanced but were similar in the young normotensive and hypertensive subjects. In young subjects, hypertension did not affect left ventricular responses to isoproterenol alone, whereas older hypertensive subjects showed some blunting of left ventricular responses compared with older normotensive subjects. With ganglionic blockade, young hypertensive subjects also showed mild blunting of left ventricular responses. CONCLUSION: These results show that, in humans, hypertension does not lead to a decrease in chronotropic responses to infusion of the beta-agonist isoproterenol and causes only a modest decrease in left ventricular responses.

Adrenergic beta-Agonists↗
PubMed1986

Circulating catecholamines modulate ischemic brain damage.

In search of factors influencing the outcome of an ischemic insult, we induced 10 min of forebrain ischemia in rats and assessed neuronal necrosis by quantitative histopathology after 1 week of recovery. Procedures for inducing ischemia included bilateral carotid artery clamping and reduction of blood pressure to 40-50 mm Hg by bleeding. To facilitate rapid lowering of blood pressure, a ganglionic blocker, trimethaphan (TMP), was administered at the onset of ischemia. Omission of the ganglionic blocker proved to markedly ameliorate neuronal damage. Similarly favorable effects were obtained when a mixture of adrenaline and noradrenaline (1 microgram kg-1 min-1 each) was infused during the early recirculation period in animals previously given TMP. Infusion of noradrenaline alone also ameliorated the damage, though the efficacy was somewhat less. The results suggest that catecholamines, released as a response to stress, ameliorate ischemic brain damage.

Animals↗
PubMed1975

Adrenergic mechanisms in human hypertension and in spontaneously hypertensive rats.

1. The role of adrenergic neuronal mechanisms in the development of early hypertension in man and the spontaneously hypertensive rat has been explored. 2. In both, a hyperkinetic circulatory state is associated with reduced parasympathetic and increased adrenergic cardiac influences. 3. Spontaneously hypertensive and normotensive control rats were treated with propranolol from conception until 12 weeks. Although heart rate and output remained reduced, there was no difference in growth or elaboration of pressure with respect to their untreated controls. 4. After another series of spontaneously hypertensive and control rats received cardiac autonomic blockade (atropine and timolol), they sequentially received alpha-adrenergic blockade (phenoxybenzamine), ganglionic blockade (trimethaphan) and smooth-muscle vasodilatation (hydralazine). These studies revealed only a small pressure differential between the two groups before hydralazine and still less thereafter; unlike the control rats, pressure in spontaneously hypertensive rats fell markedly after ganglionic blockade as a result of reduced output, indicating greater adrenergic control mediated through venoconstriction. 5. These findings indicate: increased cardiovascular adrenergic control in young spontaneously hypertensive rats, the hyperkinetic circulation merely reflecting one aspect of increased total cardiovascular input. Structural alterations seem to participate minimally. 6. These experimental observations closely, resemble findings in early hypertensive man, and it is suggested that altered total cardiovascular adrenergic input is responsible for the elaboration, development, and maintenance of essential hypertension in man.

Animals↗
PubMed1976

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.

Blood Flow Velocity↗