mmHg In Response Research Articles

Diamox((R)) challenge test to decide indications for cerebrospinal fluid shunting in normal pressure hydrocephalus.

The indications for cerebrospinal fluid (CSF) shunting in patients with normal pressure hydrocephalus (NPH) have not been established. Establishment of clear-cut indications for this procedure is essential to ensure cost-effective, and safe treatment. We report the usefulness of the Diamox((R)) challenge test in evaluating indications for CSF shunting in patients with NPH. Pre- and post-operative responses in cerebral blood flow (CBF) and intracranial pressure (ICP) to intravenous administration of Diamox((R)) 1000mg (Diamox((R)) administration) were analysed in 41 patients with NPH who were treated by ventriculoperitoneal (VP) shunt with a programmable valve and an on-off valve. The preoperative response of ICP to Diamox((R)) administration was more than 10 mmHg in most patients in whom the shunt was effective (shunt effective group), however, it was less than 10 mmHg in most patients in whom the shunt was ineffective (shunt non-effective group). Furthermore, the postoperative response of ICP to Diamox((R)) administration decreased to less than 10 mmHg in most patients in the shunt effective group. The increases in CBF in response to Diamox((R)) administration were similar in the two groups both before and after placement of the VP shunt. Patients in whom ICP increased by more than 10 mmHg in response to Diamox((R)) administration were regarded to have poor CSF circulation and to thus be candidates for CSF shunting. The Diamox((R)) challenge test is a simple, safe procedure, useful in evaluating the response to treatment.

Endothelin-1 and CYP450 arachidonate metabolites interact to promote tissue injury in DOCA-salt hypertension.

Inhibition of cytochrome P-450 (CYP450) enzymes with cobalt chloride (CoCl2) prevented hypertension, organ hypertrophy, and renal injury induced by DOCA and salt (1% NaCl) in uninephrectomized (UNx) rats. Systolic blood pressure (SBP) rose to 193 +/- 6 mmHg by day 21 from control levels of 150 +/- 7 mmHg in response to DOCA-salt treatment, a rise that was prevented by CoCl2 (24 mg. kg-1. 24 h-1). The effects of DOCA-salt treatment, which increased protein excretion to 88.3 +/- 6.9 mg/24 h on day 21 from 9.0 +/- 1.1 mg/24 h on day 3, were prevented by CoCl2. CoCl2 also attenuated the renal and left ventricular hypertrophy and the increase in media-to-lumen ratio in hypertensive rats. DOCA-salt treatment increased excretion of endothelin (ET)-1 from 81 +/- 17 to 277 +/- 104 pg. 100 g body wt-1. 24 h-1 associated with a fourfold increase in 20-hydroxyeicosatetraenoic acid (20-HETE) excretion from 3.0 +/- 1.1 to 12.2 +/- 1.9 ng. 100 g body wt-1. 24 h-1 (days 3 vs. 21). CoCl2 blunted these increases by 58 and 72%, respectively. In aortic rings pulsed with [3H]thymidine, ET-1 increased its incorporation. Dibromododec-11-enoic acid, an inhibitor of 20-HETE synthesis, attenuated ET-1-induced increases in [3H]thymidine incorporation. We distinguished effects of CoCl2 acting via CO generation vs. suppression of CYP450-arachidonic acid metabolism by treating UNx-salt-DOCA rats with 1-aminobenzotriazole (ABT), which suppresses CYP450 enzyme activity, and compared these results to those produced by CoCl2. ABT reduced hypertension, as did CoCl2. Unlike CoCl2, ABT did not prevent organ hypertrophy and proteinuria, suggesting that these effects were partially related to CO formation. Blockade of the ETA receptor with BMS-182874 reduced SBP, organ hypertrophy, and proteinuria, indicating the importance of ET-initiated abnormalities to the progression of lesions in UNx-salt-DOCA.

Altered renal hemodynamics and impaired myogenic responses in the fawn-hooded rat.

The present study examined whether an abnormality in the myogenic response of renal arterioles that impairs autoregulation of renal blood flow (RBF) and glomerular capillary pressure (PGC) contributes to the development of renal damage in fawn-hooded hypertensive (FHH) rats. Autoregulation of whole kidney, cortical, and medullary blood flow and PGC were compared in young (12 wk old) FHH and fawn-hooded low blood pressure (FHL) rats in volume-replete and volume-expanded conditions. Baseline RBF, cortical and medullary blood flow, and PGC were significantly greater in FHH than in FHL rats. Autoregulation of renal and cortical blood flow was significantly impaired in FHH rats compared with results obtained in FHL rats. Myogenically mediated autoregulation of PGC was significantly greater in FHL than in FHH rats. PGC rose from 46 +/- 1 to 71 +/- 2 mmHg in response to an increase in renal perfusion pressure from 100 to 150 mmHg in FHH rats, whereas it only increased from 39 +/- 2 to 53 +/- 1 mmHg in FHL rats. Isolated perfused renal interlobular arteries from FHL rats constricted by 10% in response to elevations in transmural pressure from 70 to 120 mmHg. In contrast, the diameter of vessels from FHH rats increased by 15%. These results indicate that the myogenic response of small renal arteries is altered in FHH rats, and this contributes to an impaired autoregulation of renal blood flow and elevations in PGC in this strain.

Glucose and Fatty Acid Oxidation by the In Situ Dog Heart During Experimental Cooling and Rewarming

Background. Reduced myocardial function after hypothermia may be metabolic in origin, but the relationship between myocardial metabolism and the various components of hypothermia-mediated dysfunction has not been thoroughly investigated. Methods. In the present study we measured myocardial uptake and oxidation of glucose and oleate in mongrel dogs undergoing cooling to 25°C followed by rewarming to 37°C, using radiolabeled substrates. Results. Segment work index declined from 39.3 ± 5.1 to 15.1 ± 2.4 mm Hg in response to cooling from 37° to 25°C and did not recover completely on rewarming (27.2 ± 4.2 mm Hg, p < 0.05). Oleate uptake declined from 3,251 ± 619 to 1,043 ± 356 nmol · min −1 · 100 g −1 ( p < 0.05) when the dogs were cooled from 37° to 25°C. Simultaneously, oxidation rate fell from 1,089 ± 158 to 354 ± 83 nmol · min −1 · 100 g −1 ( p < 0.05). On rewarming, oleate uptake was restored to prehypothermic values, whereas its rate of oxidation remained depressed (480 ± 129 nmol · min −1 · 100 g −1; p < 0.05). Uptake and oxidation of glucose also declined significantly during cooling. However, both uptake and oxidation of glucose recovered fully on rewarming. Conclusions. The results of the present study demonstrate a reduced capacity to oxidize fatty acids by the myocardium during rewarming after hypothermia.

CO2 asphyxia increases plasma norepinephrine in rats via sympathetic nerves.

The objective of this study was to determine whether the plasma norepinephrine (NE) increase in rats exposed to CO2 asphyxia was due to adrenal gland release or sympathetic nerve ending (SNS) release. Plasma NE was measured by high-performance liquid chromatography in hypertensive and normotensive rats using the following protocol: control session, CO2 exposure, N2 exposure, reserpine + CO2, and adrenalectomy + CO2. Four strains of male and female rats were used: spontaneously hypertensive rats, Wistar-Kyoto rats, and two congenic strains with different Y chromosomes. The same rats were used throughout the experiment (n = 80). Blood pressure measured by aortic telemetry increased approximately 50-60 mmHg in response to CO2 in all strains. CO2 increased NE 6-10x in all strains and both genders. N2 produced a significant increase in NE (73% of CO2 response). Reserpine significantly decreased (67%) plasma NE after CO2. Adrenalectomy did not significantly reduce the NE response to CO2. In conclusion, the increase in plasma NE after CO2 was associated with SNS release and not adrenal medullary release, was mainly due to hypoxia, and was not a specific response to CO2.

Foot TcPO 2 Response to Lumbar Sympathectomy in Patients with Focal Ischemic Necrosis

We prospectively evaluated all patients with superficial foot necrosis of 1-3 cm and transcutaneous oxygen tension (TcPO2) values of <30 mmHg who received a sympathectomy as the primary treatment of their vascular occlusive disease. Preoperatively, and every 2-3 days in the postoperative period, measurement of TcPO2 of the forefoot was performed. Clinical success was defined as healing of the necrosis or healing of a toe amputation and avoidance of a major below-knee/above-knee amputation for 1 year. Ten patients were available for long-term evaluation. During the first 4-5 days, all patients increased their foot TcPO2 and the mean increase (23 mmHg) was significant (p = 0.04). Clinical improvement was marked by an average increase of 29 mmHg by postoperative day 10. In contrast, patients with clinical failure had only an average increase of 5 mmHg in TcPO2 by the same postoperative interval. Preoperative increase in TcPO2 by at least 20 mmHg in response to dependency predicted a favorable response to sympathectomy. In addition, sustained postoperative increases in tissue oxygen levels by postoperative day 10 also favored wound healing.

Effects of rapid colloid volume expansion on pulmonary microvascular pressure and lung water in the conscious sheep

Increased pulmonary microvascular pressure (P mv), in combination with other factors, may cause pulmonary interstitial oedema. Whether increased P mv alone induces alveolar oedema is questionable. In the present study we used the heavy water-indocyanine green dilution method to measure lung water during a rapid intravascular volume expansion in the sheep. Eight conscious sheep were given two 10-min intravenous infusions of either 50 ml/kg ( N=2) or 35 ml/kg ( N=6) of dextran 60 with an interval of 10 min between them. At a P mv of 40 mmHg, respiratory distress was observed in sheep no. 2 which had been given a total amount of 100 ml/kg of dextran; this was immediately followed by a lethal pulmonary haemorrhage. Mean P mv in the remaining seven sheep increased to 31 (7) mmHg in response to the volume expansion without causing any respiratory distress or increase in lung water. These results show that in conscious sheep the lungs have strong protective mechanisms against hydrostatic oedema. They do not support the hypothesis that increased P mv alone induces alveolar oedema, but suggest that an increase in P mv to 40 mmHg may cause stress failure of the pulmonary vasculature.

PGF 2 α/pilocarpine interactions on IOP and accommodation in monkeys

We investigated whether (i) single or repeated topical treatment with either the tromethamine salt or the isopropyl ester of prostaglandin F2 alpha (PGF2 alpha-TS or PGF2 alpha-IE) inhibits the accommodative response to pilocarpine; (ii) pilocarpine given after PGF2 alpha inhibits the latter's ocular hypotensive effect, as occurs with the reverse order of administration. PGF2 alpha-IE (2 micrograms) or PGF2 alpha-TS (50 micrograms) was applied topically to the right eye of five cynomolgus monkeys twice daily for 4 days. Before initial dosing, and 1 hr after the initial and final dose the animals were anesthetized with ketamine, and intraocular pressure (IOP) and refraction determined bilaterally. Following post-PG IOP and refraction determinations, pilocarpine HCl was given topically (bilaterally) or infused i.m. over 10 min, after which refraction was determined periodically for 50 min. IOP was then again determined. After a single unilateral dose of PGF2 alpha-TS or PGF2 alpha-IE, IOP was unchanged. Both eyes accommodated markedly and equally in response to pilocarpine, and IOP fell bilaterally by a statistically significant 3 mmHg in response to pilocarpine. Repeated doses of PGF2 alpha-TS or PGF2 alpha-IE did not significantly affect the accommodative response to pilocarpine, while pilocarpine did not alter the approximately 10 mmHg ipsilateral IOP fall induced by repeated dosing of PGF2 alpha-TS or PGF2 alpha-IE. It is concluded that repeated unilateral topical application of PGF2 alpha-TS or PGF2 alpha-IE to the cynomolgus monkey eye markedly reduces ipsilateral IOP, but has no effect on the ipsilateral or contralateral eye accommodative response to pilocarpine. Pilocarpine reverses the PGF2 alpha-TS or PGF2 alpha-IE-induced fall in IOP when given before the PGF2 alpha, but does not prevent it when given after, within the parameters of this study.

Perfusion of the preoptic area with muscimol or prostaglandin E 2 stimulates cardiovascular function in anesthetized rats

The effect of unilateral perfusion of the preoptic area (POA) utilizing in vivo microdialysis with the GABAergic agonist, muscimol, or prostaglandin E 2 (PGE 2) on cardiovascular function (heart rate, blood pressure and cutaneous blood flow) was determined in halothane-anesthetized rats. Perfusion of muscimol or PGE 2 increased the heart rate, 55 ± 6 beats/ min and 69 ± 12 betas/min, respectively ( P < 0.01). Cutaneous paw blood flow tended to decrease. Blood pressure did not change in response to the perfusion of muscimol, but increased 9 mmHg in response to the perfusion of PGE 2 ( P < 0.01). The increases in heart rate and blood pressure were blocked by systemic administration of propranolol or adrenalectomy ( P < 0.01), suggesting that these effects were due to the activation of the sympathetic innervation of the heart or adrenal gland. It is proposed that the POA provides a tonic inhibitory afferent to posterior hypothalamus neurons which regulate cardiovascular function.

Distribution and functional significance of cardiac angiotensin converting enzyme in hypertrophied rat hearts.

The intracardiac conversion rate of angiotensin (Ang) I to Ang II and the expression of angiotensin converting enzyme (ACE) mRNA are amplified in rat hearts with left ventricular hypertrophy (LVH). To examine whether the accelerated intracardiac Ang II generation in LVH is related to an induction of cardiac ACE, we studied localization and function of cardiac ACE in hypertrophied rat hearts using specific ACE inhibitors. Cardiac ACE was localized and quantified in hearts from male Wistar rats with LVH due to chronic experimental aortic stenosis and from control rats. With the ACE inhibitor 125I-351A, a derivative of lisinopril, as a radioligand on coronal sections of LVH and control hearts, in vitro autoradiography demonstrated ACE binding in aorta, coronary arteries, atria, and ventricles of both groups. Quantitative analyses revealed that ACE density (counts per minute per cross-sectional area of tissue) was twofold higher within the myocardium of hypertrophied left ventricles compared with controls (p < 0.005). Quantitative morphometry demonstrated a modest increase in the fractional volume of myocytes as well as capillary volume without an increase in the fractional volume of endothelial cells in left ventricular tissue from aortic stenosis rats. These data suggest that an increase in endothelial cell volume per se cannot alone account for the observed doubling of ACE density and support an upregulation of ACE production in hypertrophied tissue. The role of cardiac ACE in intracardiac conversion of Ang I to Ang II and its specific inhibition was studied in isolated, isovolumic beating, buffer-perfused LVH and control hearts. Biochemical conversion rates as well as functional changes in response to 3 x 10(-7) M Ang I were examined in the absence or presence of the ACE inhibitor enalaprilat (4 x 10(-6) M). After a brief stabilization period, groups of LVH and control hearts were subjected to the following infusion protocols: 15 minutes of vehicle followed by 30 minutes of Ang I plus vehicle, 15 minutes of enalaprilat followed by 30 minutes of Ang I plus enalaprilat (enal/Ang I), or 45 minutes of vehicle only to allow comparison with a time control. Intracardiac Ang I-to-Ang II conversion rate was fourfold higher in LVH than in control hearts (p < 0.05). Infusion of enalaprilat reduced the intracardiac Ang I-to-Ang II conversion rate in LVH hearts by 70% (p < 0.05 versus Ang I). At similar levels of constant coronary flow per gram, Ang I increased coronary perfusion pressure by 23 +/- 5 mm Hg (p < 0.01 versus vehicle) in LVH hearts and by 36 +/- 10 mm Hg (p < 0.005 versus vehicle) in control hearts. When enalaprilat was infused with Ang I, the increase in perfusion pressure was limited to 5 +/- 5 mm Hg (NS versus vehicle) in LVH hearts and 12 +/- 3 mm Hg (p < 0.05 versus vehicle) in control hearts and was significantly lower than in hearts infused with Ang I only (p < 0.05 in LVH and p < 0.05 in control hearts, respectively). Systolic function was not affected by either infusion protocol. In contrast, Ang I infusion was associated with diastolic dysfunction. In LVH hearts, left ventricular end-diastolic pressure (LVEDP) increased from 10 +/- 1 mm Hg at baseline to 25 +/- 2 mm Hg at the end of the Ang I infusion (p < 0.001 versus vehicle), which was inhibited by infusion of enalaprilat. In control hearts, there was a lesser increase in LVEDP from 10 +/- 1 mm Hg to 15 +/- 1 mm Hg in response to Ang I (p < 0.05 versus LVH). Control hearts treated with enalaprilat with Ang I displayed no increase in LVEDP: These observations indicate that ACE protein is increased within the myocardium of LVH hearts, extending recent findings of increased cardiac ACE activity and mRNA levels in this model of pressure-overload LVH in the rat. Blockade of the enzyme by an ACE inhibitor decreases intracardiac Ang I-to-Ang II conversion rate and prevents the functional changes of Ang I-to-Ang II activation

Cardiovascular Response During Postural Change in the Elderly

In order to evaluate the heart rate and blood pressure response during sitting and standing, as well as during the change from sitting to standing, we studied 40 healthy men and women, aged 60-76 years, by means of a noninvasive beat-to-beat blood pressure tracking cuff. Heart rate and blood pressure curves immediately after standing exhibited pronounced flattening relative to a younger population, with no differences between men and women. Only four subjects showed systolic blood pressure drops of at least 15 mmHg in response to standing. Both handgrip and mental arithmetic significantly modified the cardiovascular response from sitting to standing, raising the possibility that individuals with orthostatic hypotension and impaired circulatory reflexes could be trained to utilize behavioral techniques as a means of preventing blood pressure from dropping too far during orthostasis.

副交感神経系機能低下の関与が考えられた超高齢者起立性低血圧の一症例

94-year-old male patient, with orthostatic hypotension, possibly due to impairment of vasoconstriction and parasympathetic nervous system dysfunction was reported. This patient experienced faintness and lower muscle weakness on standing. The blood pressure was 180/90 mmHg in a supine position, while it significantly decreased to 100/58 mmHg in an upright position. There was no evidence indicating the presence of organic brain diseases, cardiovascular diseases, and endocrine diseases, plasma catecholamine, renin, aldosterone, and vasopressin levels at rest were within normal range. Thus, the cause of orthostatic hypotension of this patient was unknown. His systolic blood pressure decreased by 70 mmHg, and his diastolic blood pressure also decreased by 25 mmHg in response to a 70 degrees head-up tilting test (170/71-100/46 mmHg). Plasma vasopressin level significantly increased in response to this test (0.62-67.2 pg/ml). Plasma catecholamine levels also increased (Adr 0.01-0.10 ng/ml, Ndr 0.05-0.22 ng/ml). Other autonomic nervous system examinations revealed normal responses to mental arithmetic test, hyperventilation test, cold pressure test, and adrenalin test. However, the results of the carotid occlusion test, acetylcholine test, atropine test, phenylephrine test were considered to be abnormal. From these findings, we concluded that the functions of sympathetic nervous system were almost intact, while the parasympathetic functions were impared in this case. The orthostatic hypotension of the patient as effectively treated with fludrocortisone. This report suggests that impairment of vasoconstriction and parasympathetic neurodysfunction might be involved in the development of orthostatic hypotension in the elderly.

Attenuation of fructose-induced hypertension in rats by exercise training.

This study was initiated to see if the insulin resistance, hyperinsulinemia, and hypertension that follow feeding normotensive Sprague-Dawley rats a fructose-rich diet could be prevented by letting rats run spontaneously in exercise wheel cages. Blood pressure in sedentary rats increased from (mean +/- SEM) 125 +/- 2 to 148 +/- 3 mm Hg in response to 2 weeks of a high fructose diet, and this increment was significantly (p less than 0.001) attenuated in exercising rats (from 121 +/- 1 to 131 +/- 2 mm Hg). In addition, mean (+/- SEM) plasma insulin concentration was lower in fructose-fed rats allowed to run spontaneously (44 +/- 2 vs 62 +/- 5 microU/ml; p less than 0.01). Finally, resistance to insulin-stimulated glucose uptake was assessed by determining the steady state plasma glucose response to a continuous glucose and exogenous insulin infusion during a period in which endogenous insulin secretion was suppressed. The results of these studies indicated that the mean (+/- SEM) steady state plasma glucose concentration was significantly lower in the exercise-trained rats (127 +/- 5 vs 168 +/- 6 mg/dl; p less than 0.001), despite the fact that the steady state plasma insulin levels were also lower in rats allowed to run spontaneously (75 +/- 4 vs 90 +/- 5 microU/ml; p less than 0.05). Thus, the ability of exercise-trained rats to stimulate glucose disposal was enhanced as compared with that of sedentary rats fed the same fructose-rich diet. These data demonstrate that the insulin resistance, hyperinsulinemia, and hypertension produced in normotensive rats by feeding them a high fructose diet can be attenuated if rats are allowed to run spontaneously.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiovascular and dipsogenic effects of angiotensin II administered i.c.v. in Long-Evans and Brattleboro rats

The concurrent cardiovascular and dipsogenic effects produced by i.c.v. administration of angiotensin II (AII) have been investigated in vasopressin-deficient (Brattleboro) and control (Long-Evans) rats. When animals were allowed to drink during testing, the pressor effect of i.c.v. AII (500 ng) in Long-Evans rats(26 ±3/26± 3mm Hg) was significantly greater than that produced when drinking water was not available(19 ±2/18± 2mm Hg). There was a significant decrease in heart rate only when water was available. There was no pressor response to i.c.v. AII in Brattleboro rats not allowed to drink, whereas blood pressure increased by17 ±3/14± 1 mm Hg in response to i.c.v. AII when drinking water was present. There were no significant changes in heart rate following i.c.v. AII in Brattleboro rats. When baseline drinking was taken into account, Brattleboro rats still drank significantly more water than Long-Evans rats in response to i.c.v. AII. Pretreatment of Long-Evans rats with the V 1 vasopressin antagonist, d(CH 2) 5Tyr(Et)DAVP, decreased the pressor effect of i.c.v. AII to a level not significantly different from that of Brattleboro rats allowed to drink. Under these conditions the amount drunk by Long-Evans rats was not significantly less than that drunk by Brattleboro rats. These results confirm that the central pressor actions of AII are mediated, in part, by release of vasopressin and suggest that the greater dipsogenic effect of i.c.v. AII in Brattleboro compared with Long-Evans rats may be due, partly, to its lesser pressor activity in these animals.

Long-term effects of betamethasone on blood pressure and hypothalamo-pituitary-adrenocortical function in spontaneously hypertensive and normotensive rats.

An enhanced hypothalamo-pituitary-adrenocortical (HPA) activity has been described during onset of elevated blood pressure in spontaneously hypertensive rats (SHR). An instability of the HPA axis could thus contribute to the development of hypertension in these animals. Glucocorticoid effects on blood pressure and HPA function were studied therefore in SHR and normotensive Wistar-Kyoto (WKY) and Wistar rats. Beginning at 4 weeks of age, the rats were treated with 0.1 and 0.5 microgram betamethasone per milliliter drinking water for 7 weeks. SHR and WKY responded with a significant elevation in average blood pressure. In SHR, mean blood pressure rose from 181.4 +/- 3.9 (mean +/- SEM) to 203.1 +/- 2.8 mm Hg in response to the lower dose of betamethasone and to 209.2 +/- 4.0 mm Hg in response to 0.5 microgram betamethasone per milliliter drinking water. In WKY, blood pressure increased from 134.4 +/- 3.3 to 148.2 +/- 3.0 and 157.9 +/- 4.5 mm Hg in response to the lower and higher dose of betamethasone, respectively. No significant effect was seen in Wistar rats, where the mean blood pressure values changed insignificantly from 133.8 +/- 2.1 to 136.3 +/- 3.2 and 135.6 +/- 2.4 mm Hg. Stress-induced secretion of corticosterone was significantly suppressed in a dose-dependent manner in all three strains. Stress-induced secretion of adrenocorticotropin was markedly reduced by 0.5 microgram betamethasone per milliliter in SHR and by both doses in WKY. No significant effect, however, was seen in Wistar rats. A predisposition to the hypertensiogenic actions of glucocorticoids was found therefore in SHR and WKY, but not in Wistar rats.

Effect of the angiotensin II blocker 1-Sar-8-Ala-angiotensin II on renal artery clip hypertension in the rat.

Twenty-four conscious male Wistar rats with hypertension induced by left renal artery clipping (two-kidney hypertension) were infused intravenously with 1-Sar-8-Ala-angiotensin II a competitive angiotensin II antagonist. The spectrum of responses was wide, ranging from a mild elevation in blood pressure to a marked fall in blood pressure, despite effective and specific angiotensin blockade in all cases. The change in blood pressure during 1-Sar-8-Ala-AII infusion activity showed a significant correlation with the level of plasma renin prevailing immediately before the infusion (r = - 0.78, P less than 0.01) but not with the prevailing blood urea level (r = 0.27, 0.1 greater than P greater than 0.05), the drgree of hypertension (r = 0.42, 0.1 greater than P greater than 0.05), or the time since clipping (r = 0.02, P greater than 0.05). There was no significant correlation between the degree of hypertension and the plasma renin activity (r = 0.42, 0.1 greater than P greater than 0.05). In rats with blood pressure drops greater than 20 mm Hg in response to 1-Sar-8-Ala-AII, the final blood pressure level was still above the normotensive range. Excision of the clipped kidney reduced blood pressure to normal or to near normal within 24 hours in all of the rats tested. It is concluded that the degree of dependence of renal hypertension on the renin-angiotensin system is directly related to the increase in circulating angiotensin itself and not to an increase in sensitivity to angiotensin. Other factors appear to be involved in renal clip hypertension in addition to circulating renin and angiotensin, especially when the measured activity of plasma renin is normal.

The "Pressor Reflex" of Bladder Origin : STUDY OF A CASE WITH HYPERACTIVE "PRESSOR REFLEX" OF BLADDER ORIGIN, BILATERAL HYDRONEPHROSIS POSSIBLY COMPLICATED WITH PYELONEPHRITIS, AND THE STRICTURE OF THE URETHRA

The authors describe a patient who may be taken to represent a man with abnormally hyperactive "pressor reflex" in response to the distension of the bladder in spite of the absence of gross injury to the spinal cord. His blood pressure rose by 45/25 mmHg in response to the physiological and slow artificial distension of the bladder. Besides this peculiarity, this patient had urographic evidences of the bilateral hydronephrosis presumably complicated with chronic pyelonephritis, and hypertension possibly through this renal mechanism and possibly O'conor type hypertension.