Blood Pressure In Animals Research Articles

Blood pressure monitoring in zoologically managed bonobos (Pan paniscus).

In response to the growing evidence that hypertension may play a significant role in the development of cardiovascular disease (CVD) in bonobos, the Great Ape Heart Projectestablished a finger blood pressure (BP) monitoring protocol for zoo-housed bonobos. The ability to monitor BP without the use of anesthesia provides more opportunities to detect potential hypertension in its early stages allowing for therapeutic intervention that may slow the progression of CVD. No BP reference ranges exist for bonobos due to the lack of an established protocol, the difficulty of measuring BP in animals, and small sample size of zoo-housed bonobos. By working with all 8 institutions in North America that care for bonobos, it was possible to (1) investigate the feasibility of using finger BP devices, and (2) establish BP trends for male and female bonobos. Data were collected from May 2016 to March 2019. Zoos were asked to train for and collect BP measurements from any bonobos willing to participate, regardless of age, sex, or health status as well as to report on the quality of the training and measurements obtained. At the start of the study, the North American bonobo population consisted of 74 bonobos ages 5 years and older at 8 institutions. All 8 institutions submitted at total of 3656 BP readings from 50 bonobos (n = 23 females, n = 27 males; ages 5-51 years) representing 67.57% of the trainable population ages 5 years and older. Of the readings submitted, 2845 were determined to be good quality, reliable BP readings (77.81% useful BP measurements) for 36 of the 50 adult bonobos submitted for this study (59.01% of the adult population ages 10-51 years) but showed limitations in the protocol for the younger population. BP trend analysis showed significant differences between bonobos that were not on medication versus those treated with cardiac medications, with those on cardiac mediations having significantly higher systolic arterial pressure, diastolic arterial pressure, and mean arterial pressure(p ≤ 0.001 for all comparisons). Systolic BP generally increased over age classes (10-19, 20-29, 30-39, 40+ years).

Blood pressure variability — regular and irregular waves

The review presents data on regular and irregular waves of blood pressure (BP) recorded during its invasive (intra-arterial) and non-invasive registration. Regular pulse waves, Traube-Hering waves (second-order waves) and Mayer waves (third-order waves) are described. The characteristic of circadian and ultradian super slow waves is given. The role of the sympathetic nervous system in the origin of regular waves of BP and their relationship with the magnitude of the baroreceptor reflex are shown. Attention is drawn to the role of changes in the minute volume of blood circulation and peripheral resistance to blood flow in the occurrence of fluctuations in BP. We also review the methods and features of BP registration, which enable identification and analysis of irregular high-frequency fluctuations in BP, the relationship of these fluctuations with the magnitude of the baroreceptor reflex and the activity of the sympathetic nervous system. The data on the amplitude of high-frequency irregular fluctuations in BP in animals with simulated hypertension are presented. The review draws attention to the possibility of recording regular fluctuations in BP during its constant non-invasive registration.

Goat meat does not cause increased blood pressure.

While there are persistent rumors that the consumption of goat meat dishes increases blood pressure, there is no scientific evidence to support this. Two experiments were conducted to clarify whether or not blood pressure increases in conjunction with the consumption of goat meat dishes. In experiment 1, 24 Dahl/Iwai rats (15 weeks old, body weight 309.3±11.1 g) were evenly separated into 4 groups. The control group (CP) was fed a diet containing 20% chicken and 0.3% salt on a dry matter basis. The goat meat group (GM) was fed a diet containing 20% goat meat and 0.3% salt. The goat meat/salt group (GS) was fed a diet containing 20% goat meant and 3% to 4% salt. The Okinawan mugwort (Artemisia Princeps Pampan)/salt group (GY) was fed a diet containing 20% goat meat, 3% to 4% salt and 5% of freeze-dried mugwort powder. The experiment 1 ran for a period of 14 weeks during which time the blood pressure of the animals was recorded. The GS, and GY groups consumed significantly more water (p<0.01) than the CP and GM groups despite the fact that their diet consumption levels were similar. The body weight of animals in the CP, GM, and GS groups was similar while the animals in the GY group were significantly smaller (p<0.01). The blood pressure in the GM group was virtually the same as the CP group throughout the course of the experiment. In contrast, while the blood pressure of the animals in the GS and GY group from 15 to 19 weeks old was the same as the CP group, their blood pressures were significantly higher (p<0.01) after 20 weeks of age. The GY group tended to have lower blood pressure than the GS group. In experiment 2, in order to clarify whether or not the increase in blood pressure in the GS group and the GY group in experiment 1 was caused by an excessive intake of salt, the effects on blood pressure of a reduction of salt in diet were investigated. When amount of salt in the diet of the GS and GY group was reduced from 4% to 0.3%, the animal’s blood pressure returned to normotensive. These results indicate that, as in the case of chicken consumption, prolonged consumption of goat meat does not cause increased blood pressure, rather the large amount of salt used in the preparation of goat meat dishes is responsible for the increase in blood pressure.

Central interactions of aldosterone and angiotensin II in aldosterone- and angiotensin II-induced hypertension

Many studies have implicated both angiotensin II (ANG II) and aldosterone (Aldo) in the pathogenesis of hypertension, the progression of renal injury, and cardiac remodeling after myocardial infarction. In several cases, ANG II and Aldo have been shown to have synergistic interactions in the periphery. In the present studies, we tested the hypothesis that ANG II and Aldo interact centrally in Aldo- and ANG II-induced hypertension in male rats. In rats with blood pressure (BP) and heart rate (HR) measured by DSI telemetry, intracerebroventricular (icv) infusions of the mineralocorticoid receptor (MR) antagonists spironolactone and RU28318 or the angiotensin type 1 receptor (AT1R) antagonist irbesartan significantly inhibited Aldo-induced hypertension. In ANG II-induced hypertension, icv infusion of RU28318 significantly reduced the increase in BP. Moreover, icv infusions of the reactive oxygen species (ROS) scavenger tempol or the NADPH oxidase inhibitor apocynin attenuated Aldo-induced hypertension. To confirm these effects of pharmacological antagonists, icv injections of either recombinant adeno-associated virus carrying siRNA silencers of AT1aR (AT1aR-siRNA) or MR (MR-siRNA) significantly attenuated the development of Aldo-induced hypertension. The immunohistochemical and Western blot analyses of AT1aR-siRNA- or MR-siRNA-injected rats showed a marked reduction in the expression of AT1R or MR in the paraventricular nucleus compared with scrambled siRNA rats. When animals from all studies underwent ganglionic blockade with hexamethonium, there was a smaller reduction in the fall of BP in animals receiving icv AT1R or MR antagonists. These results suggest that ANG II and Aldo interact in the brain in a mutually cooperative manner such that the functional integrity of both brain AT1R and MR are necessary for hypertension to be induced by either systemic ANG II or Aldo. The pressor effects produced by systemic ANG II or Aldo involve increased central ROS and sympathetic outflow.

Comparative Hemodynamic Effects of Levosimendan Alone and in Conjunction with 4-Aminopyridine or Calcium Chloride in a Rodent Model of Severe Verapamil Poisoning

Levosimendan (Levo) increases sensitivity of troponin-C to calcium, thus increasing myocardial contractility. It is also a vascular K+-ATP channel agonist producing peripheral vasodilation. Previous research with levosimendan revealed an increase in cardiac output (CO) but not blood pressure (BP) in experimental verapamil poisoning. Levosimendan's K+-channel agonist properties may augment verapamil's vasodilatory effects. 4-Aminopyridine (4-AP) is a K+-channel antagonist. It has successfully reversed hypotension in experimental verapamil poisoning. We hypothesized that coadministration of these agents may improve BP and CO in verapamil poisoning. Anesthetized, ventilated, and canulated male Wistar rats were poisoned with verapamil. Animals received one of six treatments, which are as follows: (1) n-saline infusion (control), (2) Levo 6.25 μg/kg loading dose and 36 μg/kg/h infusion, (3) 4-AP 2 mg/kg loading dose and infusion (4-AP), (4) Levo+4-AP, (5) CaCl₂ loading dose and infusion, and (6) Levo+CaCl(2). Hemodynamic parameters were recorded for 60 min. Outcome measures were changes in CO, BP, and heart rate (HR) compared to control. All groups had similar pretoxicity and peak toxicity CO (50% of pretoxicity value), BP (50% or pretoxicity value), and HR. Control group CO, BP, and HR progressively dropped during the verapamil infusion. Levosimendan produced a statistically significant improvement in CO (75% of pretoxicity level) but not BP in comparison to control. 4-AP produced a significant improvement in CO (110% of pretoxicity) and BP (78% of pretoxicity). Levo+4-AP and Levo+CaCl₂ groups improved CO (100% of pretoxicity) and BP (77% and 50% of pretoxicity, respectively), but there was no additive increase in CO or BP in animals compared to 4-AP or CaCl₂ alone. Levosimendan moderately improved CO but not BP in verapamil poisoning. The hypotensive effects of levosimendan were not overcome by coadministration of either 4-AP or CaCl₂. Levosimendan may not be an appropriate agent to use in the treatment of verapamil poisoning.

Activation Of Adenosine A2A Receptors Causes Hypotension In Newborn But Not Adult Rats

Hypotension is very common in premature infants and has been associated with poor neurodevelopmental outcome although the underlying pathophysiology is unclear. Activation of central adenosine A2A receptors in decerebrate, vagotomized newborn piglets caused hypotension. We hypothesized that over‐expression of adenosine A2A receptors predisposes newborns to hypotension. We aimed to test this hypothesis by examining the effect of intraperitoneal injection (IP) of adenosine A2A receptor agonist CGS 21680 (CGS) on blood pressure (BP) in awake, non‐restrained maturing rats. BP was measured using a non‐invasive cuff blood pressure system, sphygmomanometery, on rat tail (PanLab, Spain). After 30 minutes of acclimatization in appropriate size chambers BP was measured before and one hour after IP CGS (4 mg/kg). CGS caused a significant decrease in systolic and diastolic BP in animals up to 6 weeks of life (n=13) but not adult rats (n=2). The systolic and diastolic BP decreased from 118±4 and 83±3 mmHg before CGS to 96±5 and 65±3 mmHg after CGS, respectively, p &lt;0.001. Additionally, CGS caused a significant increase in heart rate from 426±7 to 528±14 before and after CGS, respectively, p &lt; 0.001. We conclude that activation of adenosine A2A receptors causes hypotension in young but not adult rats. We speculate that over‐expression of adenosine A2A receptors early in life predisposes preterm infants to hypotension.

A vitamin-E-fortified diet reduces oxidative stress, sympathetic nerve activity, and hypertension in the phenol-renal injury model in rats

Renal injury caused by the injection of phenol in the lower pole of one kidney increases sympathetic nervous system (SNS) activity and blood pressure (BP), and these effects are mediated by increased reactive oxygen species (ROS) in brain nuclei involved in the noradrenergic control of BP. This suggests that therapy with antioxidants might be beneficial in this model. In this study, we tested the hypothesis that a vitamin (Vit)-E-enriched diet might decrease oxidative stress in the brain and result in reduced SNS activity and BP in animals with phenol-renal injury. To this end, we examined the effects of a Vit-E-fortified diet vs. a control diet on BP, norepinephrine (NE) secretion from the posterior hypothalamic nuclei (PH), and the abundance of several components of Nicotinamide Adenine Dinucleotide Phosphate (NADPH) oxidase in the brain of rats with phenol-induced renal injury. A Vit-E-fortified diet mitigated the formation of ROS in the brain, and this was associated with reduced SNS activity and BP in rats with phenol-induced renal injury. In conclusion, antioxidants appear to be beneficial in the management of hypertension caused by renal injury and increased SNS activity.

Potential of Gene Therapy Strategy for the Treatment of Hypertension

Hypertension is one of the most important risk factors for cardiovascular diseases (CVDs). CVD extends across all populations and represents the leading cause of morbidity and mortality in industrialized countries. Hypertension increases the risk of peripheral arterial disease, cardiomyopathy, stroke, and renal failure. The disease affects &50 million Americans and goes undetected in at least one third of the population. In spite of the tremendous progress made by pharmacotherapy in the management and control of hypertension, there has been a steady escalation in its prevalence during the last decade. This has led many to conclude that traditional pharmacotherapy has reached an intellectual plateau and that novel and innovative approaches must be sought for the treatment, control, and possible cure of hypertension. As a result, efforts of our group and those of many others have been diverted to explore the use of gene transfer and gene therapy strategies for a long-term control of hypertension. We have argued that gene therapy offers potentially significant improvements and benefits over the use of traditional pharmacotherapy: (1) noncompliance by patients can be significantly reduced or even eliminated because of the fact that a single treatment involving gene transfer could remain effective for months or even years; (2) side effects associated with pharmacotherapy can be minimized as a result of specific targeting of a therapeutic gene in a given tissue and optimally influencing cardiovascular pathophysiology on an individual patient basis; and (3) with its potential to produce long-term beneficial outcomes in end-organ damage, the gene therapy strategy could lead to a cure of hypertension and its related pathophysiology. It is noteworthy to mention that current pharmacotherapies are often unable to reverse end-organ damage associated with hypertension. In order for the gene therapy for hypertension to be successful, one must provide conceptual support of its efficacy in …

Differential Behavior of Simple and Complex Cells in Visual Cortex during a Brief IOP Elevation

To study and compare responses of different types of cortical neurons in the primary visual cortex in cats to grating stimuli before and during brief elevation of intraocular pressure (IOP). Single-unit electrophysiological recordings were performed in anesthetized and paralyzed cats. The IOP was elevated by injecting saline into the anterior chamber of the cat's eyes through a syringe needle. The IOP was elevated to a level at which the retinal perfusion pressure (arterial pressure minus IOP) was maintained at approximately 30 mmHg for a period of 4 minutes. The responses of simple and complex cells in the primary visual cortex to visually drifting sinusoidal gratings were measured before and during the elevation of IOP. The response amplitude of all the cortical cells in the primary visual cortex declined during a brief elevation of IOP. The decrease in the response of simple cells was always more significant than that of complex cells. The differential decrease between the two major types of cells was independent of the cell's receptive field location and cortical depth. There was a mild tendency for cells with higher preferred spatial frequencies to be more sensitive than those with lower frequencies. The preferred orientation and direction of most cortical cells remained roughly unchanged though their orientation and direction biases decreased. An increase in the animal's blood pressure, which returned the retinal perfusion pressure to a normal level, compensated for the decreased response induced by the elevation of IOP. The differential effects of a brief elevation of IOP on the response of simple and complex cells in the visual cortex are general and may originate from the retina through the lateral geniculate nucleus (LGN), where different effects of elevation of IOP are exerted on X- and Y-type retinal ganglion cells. The results may suggest differential behavior of neurons tin the parvo and magno pathways of the primate.

C- fos expression and electrolytic lesions studies reveal activation of the posterior region of Locus Coeruleus during hemorrhage induced hypotension

Bilateral electrolytic lesions in the rat Locus Coeruleus (LC) were made one or seven days before experimentation. Four hemorrhage sessions, withdrawing 10% of the blood volume per session, were performed in 5 min intervals in freely moving rats. Blood pressure (BP) was not affected by the lesions and did not drop in the first, but decreased in all subsequent hemorrhages. The decrease in BP in animals with lesion in the anterior LC was similar to the controls. However, animals with lesions in the posterior LC showed an enhanced decrease in BP during the second hemorrhage, in acute and chronic experiments. Expression of Fos protein was studied to investigate the relationship between LC activity and BP changes. Two hours after the second hemorrhage, the brains were removed and processed for Fos immunocytochemistry. Hemorrhage increased the number of Fos immunoreactive neurons mainly in the posterior LC. We conclude that (1) the LC does may not play a role in cardiovascular control during resting, but seems to mediate compensatory cardiovascular mechanisms in situations of hypovolemia; and (2) the posterior LC, but not the anterior, plays a pressor role during hemorrhage.

Combined effects of an angiotensin converting enzyme inhibitor and a calcium antagonist on renal injury.

Angiotensin converting enzyme inhibitors have uniformly been shown to prevent the development both of proteinuria and of glomerulosclerosis in rats with a remnant kidney. Conversely, dihydropyridine calcium antagonists (DCA) have failed to demonstrate such a benefit in spite of causing an equivalent reduction in blood pressure. To test the hypothesis that concomitant administration of an angiotensin converting enzyme inhibitor and a DCA would lead to a smaller increase both in proteinuria and in glomerulosclerosis relative to that caused by administration of a DCA alone at similar levels of blood pressure. Experiments were carried out using Sprague-Dawley rats that had been subjected to five-sixths renal ablation. Animals were allocated randomly to one of four groups: control (no treatment), amlodipine (A rats), benazepril (B rats), or a combination of benazepril and amlodipine (B + A rats). We implanted intraperitoneal sensors for telemetric monitoring of the animal's blood pressure. Other parameters measured at baseline included proteinuria and inulin clearance. After approximately 7 weeks all of the parameters were remeasured and animals killed for morphologic assessment of the kidney. The B + A rats had lower levels of proteinuria than did the rats in group A (21 +/- 12 mg/day for B + A rats versus 59 +/- 24 mg/day for A rats, P < 0.05). The degree of glomerulosclerosis in the B + A rats was also reduced markedly compared with that in A rats (12 +/- 4% for B + A rats versus 43 +/- 12% for A rats, P < 0.05). Moreover, the results on proteinuria and glomerulosclerosis of B + A rats were similar to those for B rats. These differences could not be explained totally in terms of differences in blood pressure control (144 +/- 12 mmHg in A rats versus 132 +/- 13 mmHg in B + A rats, NS). The results were consistent with the observation that a combination of benzepril and amlodipine provides additional protection against renal injury compared with that provided by amlodipine alone. The mechanism for this benefit is not known.

Free radicals may contribute to oxidative skeletal muscle fatigue

We used mouse soleus in vitro (n = 30) and canine gastrocnemius-plantaris preparations (n = 20) pump-perfused at the animal's blood pressure to establish if free radicals contribute to fatigue in oxidative skeletal muscle. The soleus from each leg contracted for 200 ms (70 Hz) once every minute for 60 min in Hepes buffer gassed with 100% oxygen at 27 degrees C. When contracting in Hepes alone, both muscles fatigued at 0.9 mN/mm2.min over the 60 min. The addition of purines to the bath increased the rate to 1.4 mN/mm2.min and the addition of xanthine oxidase to generate free radicals increased the rate again to 1.9 mN/mm2.min. Thus free radicals appeared to attenuate oxidative skeletal muscle function. Each canine muscle contracted isometrically at 4 Hz for 30 min and then rested for 45 min before contracting for a second 30 min at 4 Hz. In each experiment, we infused saline at 0.76 mL/min into resting muscle and at 1.91 mL/min during the first contraction period. During the remainder of the experiment, we infused, at the same rates, saline (n = 4), 10 microM dimethyl sulfoxide (DMSO) (n = 4) to identify the effect of scavenging hydroxyl radicals, 1 mM allopurinol to establish the effect of blocking xanthine oxidase (n = 4), or 200 microM desferoxamine to determine the effect of chelating iron (n = 4). With saline, the fatigue rate over the 30 min of contractions increased from 5.0 +/- 0.2 to 6.3 +/- 0.5 N/kg.min from the first to the second stimulation period. The fatigue rate was slower in the second period with each of the three experimental substances (DMSO, 5.9 +/- 0.8 to 3.2 +/- 0.3; allopurinol, 7.3 +/- 1.1 to 4.6 +/- 0.6; desferoxamine, 6.8 +/- 0.8 to 4.4 +/- 0.8 N/kg.min). The fatigue rate was the same as control when DMSO was infused only during the second contraction period. Therefore, free radicals appeared to contribute to fatigue in oxidative skeletal muscle.

Direct observation on microcirculation of cochlea. I. Effects of ADP and norepinephrine injections upon blood flow of radiating arteriole in guinea pigs

Blood flow at radiating arteriole of inner ear was measured with direct observations method in anesthetized guinea pigs, prior to and after drug (e. i. ADP and norepinephrine) injections into the unilateral common carotid artery. Value of blood velocity was determined from the displacement of plasma space ranning through the radiation arteriole per one second with the moving picture records.Injections of ADP 0.1 and 3mg/kg induced the decrease of blood flow and arterial blood pressure (BP), and this effect almost recovered within two min. But when a further increase of ADP dose (up to 25mg/kg or more) was given, recovery time of blood flow became prolonged or the irreversible damage was observed.A small dose of norepinephrine (0.01, 0.15mg/kg) administration produced both the increment of blood flow and arterial BP. Its increment of flow velocity was directly related to increase in systemic BP. However, a large does of norepinephrine (1.2 and 2.5mg/kg) adminis-tration led to the decrement of blood velocity irrespective of increase of BP. This phenomenon became obvious when animal's BP level was low. The dilation of blood vessel was observed after norepinephrine injection.When the blood flow velocity of radiating arteriole stopped after ADP or norepinephrine injection, its vascular lumen was completely obstructed by the aggregated red blood cells.These observations might represent one of the mechanisms of repeated human deafness and tinnitus.

Effects of Cervical Sympathetic Stimulation on Vestibulo-Ocular Reflex of Rabbits with Normal, Low and High Blood Pressure

The effect of an unilateral cervical sympathetic stimulation on per-rotational nystagmus was investigated in alert rabbits with low, normal and high blood pressure. The cervical sympathetic chain and vagus nerve on one side were cut and the distal part of the cervical sympathetic ganglion (CSG) was stimulated electrically. When a CSG was stimulated, nystagmus towards the stimulated side was suppressed predominantly. As a result, directional preponderance which was directed away from the stimulated side appeared. This effect became obvious when the animal's blood pressure was low. Oxygen partial pressure was recorded in the perilymph of inner ear and cerebellum. Unilateral CSG stimulation predominantly suppressed oxygen tension of stimulated side. This results suggested that the influence of CSG stimulation on the vestibuloocular reflex is considered to be due to aregional ischemia induced by vasoconstriction.

Studies on the Mechanism of the Enhancement of the Antihypertensive Activity of Captopril by A Diuretic in Spontaneously Hypertensive Rats

Captopril (30 mg/kg/day orally for two days) in spontaneously hypertensive rats (SHR) inhibited serum angiotensin converting enzyme (ACE) activity 92.3%; increased plasma renin activity (PRA) 18-fold and reduced mean arterial blood pressure (MABP) 19 mm Hg. Hydrochlorothiazide (HCTZ) (100 mg/kg-day 1; 10 mg/kg-day 2, orally) increased PRA 3-fold but did not affect serum ACE or MABP. HCTZ plus captopril inhibited serum ACE 95.2%; increased PRA 38-fold and reduced MABP 47.5 mm Hg. Captopril or HCTZ plus captopril did not alter the responses of isolated aortic strips to norepinephrine (NE), serotonin, angiotensin II (AII) or isoproterenol. Pressor responses of conscious SHR to AII and NE were unaltered by captopril or HCTZ plus captopril although the bradykinin-induced depressor responses were significantly but equally potentiated. These results suggest that the potentiating effect of HCTZ is due to some mechanism that shifts the animal's blood pressure maintenance system to a renin-dependent state and is not due to changes in vascular reactivity.

Effects of adenosine diphosphate administration on the vestibulo-oculomotor reflex of rabbits.

Adenosine diphosphate (ADP) injection into a unilateral vertebral artery in rabbits decreased per-rotational nystagmus; the nystagmus beating toward the injected side was predominantly suppressed. This influence became obvious when the animal's blood pressure was low. Field potentials were recorded in the vestibular nuclei upon electric stimulation of the vestibular labyrinth. ADP administration into the vertebral artery also suppressed the amplitude of vestibular evoked potentials (VEPs). Effects of ADP upon the vestibulo-ocular reflex and VEP were considered to be due to regional ischemia induced by the microemboli, which consisted of platelet aggregation.

The effects of conflict on tonic levels of blood pressure in the genetically borderline hypertensive rat.

ABSTRACTStudies of aversive conditioning in animals have seldom elicited tonic elevations in blood pressure (BP) equivalent to those which produce pathological changes in humans. While it is possible that psychological factors are not that important in the etiology of hypertension, it is also possible that the failure to elicit large tonic elevations in BP in animals may be due either to stressors which are insufficiently potent and/or to an inadequate physiological model. The present study sought to maximize the probability of producing large tonic changes in BPs by using a conflict paradignt in a genetic strain of rats which develops systolic BPs in the borderline hypertensive area (c. 150 mmHg). Forty‐eight male F1 generation offspring of spontaneously hypertensive rats mated with normotensive controls were randomly split into three groups: experimental (subjected to 3 weeks of avoidance training and 12 weeks of conflict in conditioning cages), mild restraint control (placed in conditioning cages daily but not shocked), and maturation control (neither shocked nor restrained) groups. Animals subjected to conflict gradually developed tonic levels of systolic BP well into the hypertensive range (c. 185 mmHg). Restraint control animals also showed some elevation (c. 165 mmHg), but maturational controls showed no change (c. 150 mmHg). The saliency of this animal model for the study of stress‐induced hypertension is discussed.

The relationship between sodium excretion and renin secretion by the perfused kidney.

The effect of altered tubular sodium reabsorption on renin secretion (RSR) was examined under conditions in which other factors influencing renin release could be controlled or excluded. To do this, isolated canine kidneys were perfused at constant pressure with blood circulating from donor animals. Volume expansion or hemorrhage of the donor dogs produced large changes in the animal's blood pressure, renal function, sodium excretion (UNaV), and RSR, but were without effect on renal hemodynamics, UNaV, or RSR in the perfused kidney. Hemodilution without volume expansion, resulted in hypotension, decreased UNaV and increased RSR in the donor dogs, and increased UNaV and suppressed RSR in the perfused kidney. These effects of hemodilution in the perfused kidney were partially reversed when plasma protein concentration was restored to control levels with hyperoncotic albumin, and, overall, there was a significant inverse relationship between electrolyte excretion and RSR. These results provide new evidence for the hypothesis that the rate at which sodium is delivered to the macula densa is an important determinant of the rate of renin secretion.