Transient Rise In Blood Pressure Research Articles

The therapeutic relevance of the cardiovascular response to stroke in treated and untreated Spontaneously Hypertensive Rats (SHR)

Over 80% of patients manifest a transient rise in blood pressure (BP) after ischemic stroke, regardless of their previous blood pressure level. In the spontaneously hypertensive rat (SHR), we investigate the cardiovascular response to stroke in animals already receiving chronic anti‐hypertensive treatment and evaluate the impact of actively controlling BP after stroke in these animals.Male SH rats (n=16, 374±5 g) were instrumented to allow the long‐term recording of BP and brain tissue oxygen in the penumbra (pO2) via telemetry. Resting BP was controlled for four weeks using the angiotensin‐converting enzyme inhibitor enalapril (10mg/kg/day in drinking water). After recording a 3‐day baseline, on D0, an ischemic stroke was induced via a two‐hour transient occlusion of the middle cerebral artery (MCAo). After a stroke, treatment with enalapril was continued in all rats (10mg/kg/day sc via osmotic pump) either alone (Untreated, n=8) or in conjunction with the clinically‐indicated adrenergic antagonist, labetalol (0.25mg/kg/hr sc via osmotic pump) to prevent post‐stroke hypertension (Treated n=8). Behavioural testing and neurological scoring (SHIRPA score) were performed on Days 1, 3, 7 and 10 to evaluate the functional recovery over time, and post‐mortem stroke infarct size was assessed by histology on D10.Enalapril treatment significantly and consistently reduced baseline BP to a normotensive level (from 142±1 to 116±3 mmHg, p<0.001). Following a stroke, BP increased rapidly in the Untreated rats, reaching a peak of 14±3 mmHg above baseline on Days 0 and 1 (p<0.05). Post‐stroke hypertension was successfully prevented in the Treated group, with BP significantly lower than in Untreated rats (p<0.05). Penumbra tissue oxygen levels were increased significantly above baseline in Treated animals on D1 and D2 (p<0.05), consistent with previous reports that labetalol preserves or increases cerebral blood flow despite lowering BP. Untreated and Treated rats showed a similar pattern of functional impairment and recovery after stroke, however, the infarct volume was significantly smaller in Treated animals on D10 (276±8mm3 vs Treated 220±16mm3, p<0.05).We show that a pronounced increase in BP occurs after stroke in controlled hypertensive animals. We hypothesized that this post‐stroke hypertension may be a protective response, aiding perfusion of the ischemic penumbra. Our results showed that preventing post‐stroke hypertension did not appear to have a negative impact on the functional recovery from stroke and that labetalol treatment may in fact enhance cerebral blood flow.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

A Comparative Study of Intravenous Nitroglycerin With or Without Intravenous Lignocaine for Attenuation of Stress Responses to Endotracheal Intubation

Background: Laryngoscopy and tracheal intubation lead to stress response which is characterized by transient rise in blood pressure and heart rate. This response is tolerated well in normal individuals but can lead to significant morbidity and mortality in patients with cardiovascular and cerebrovascular diseases. Search for the better drugs to suppress these responses is going on through decades.
 Aim of Study: To compare the effects of IV nitroglycerin alone and in combination with IV lignocaine, on attenuation of stress response to end tracheal intubation.
 Material and Methods: This is a randomized, double blind study conducted in 60patients admitted for operation at NGMCTH, between June 2018 to November 2018. Patients were of 16- 60 years age groups and belonging to ASA group I and II. Patients were divided into two groups: Group I IV Nitroglycerin 500 mcg+ NS 3 ml. (n=30) and Group IIIV Nitroglycerin 500 mcg+ IV Lignocaine 63 mg (n=30). Systolic Blood Pressure (SBP), Diastolic Blood Pressure (DBP), Mean Arterial Pressure (MAP) and Heart rate (HR) were measured and Rate Pressure Product (RPP) calculated.
 Results: Baseline values were comparable in both groups. Post Intubation, there was significant decrease in SBP at 0,1,3 and 5 minutes while DBP and MAP significantly decreased at 1, 3 and 5 minutes, in both groups. Significant tachycardia was noted in both groups at 0,1and 3 minutes, and RPP remained unchanged in both groups.
 Conclusion: Nitroglycerin significantly decreases blood pressure, prevents rise in RPP but does not attenuate heart rate after end tracheal intubation. There is no benefit of adding IV lignocaine to IV nitroglycerin for attenuation of stress response to end tracheal intubation.

Target organ complications and prognostic significance of alerting reaction: analysis from the Dallas Heart Study.

Noninvasive blood pressure (BP) measurement often triggers a transient rise in BP, known as an alerting reaction. However, the prevalence and prognostic significance of the alerting reaction has never been assessed in the general population. We evaluated the association between the alerting reaction and left ventricular mass by MRI and urinary albumin-to-creatinine ratio in the Dallas Heart Study, a large population sample of 3069 individuals. Participants were categorized into four groups based on levels of consecutive BP: first, normal first BP and average third to fifth (avg3-5) BP of less than 140/90 mmHg (control group); second, high first BP of at least 140/90 mmHg and normal (avg3-5) BP (alerting reaction group); third, normal first BP and high (avg3-5) BP; and fourth, high first to fifth BP. Then, associations between BP categories with incident cardiovascular outcomes (coronary heart disease, stroke, atrial fibrillation, heart failure, and cardiovascular death) over a median follow-up period of 9.4 years were assessed. The sample-weighted prevalence of isolated hypertension during the first BP measurement was 9.6%. Presence of an alerting reaction was independently associated with increased left ventricular mass, urinary albumin-to-creatinine ratio, cardiovascular events after adjustment for traditional cardiovascular risk factors, and baseline BP (adjusted hazard ratio 1.24, 95% confidence interval 1.07-1.43). Our study indicated that the alerting reaction is independently associated with increased cardiovascular and renal complications.

High salt diet increases the pressor response to stress in female, but not male ETB-receptor-deficient rats.

Acute stress in both rodents and humans causes a transient rise in blood pressure associated with an increase in plasma endothelin-1 (ET-1). High salt (HS) intake also increases ET-1 production, and interestingly, blunts the pressor response to acute air jet stress in rats. We previously reported that female rats lacking functional ETB receptors everywhere except sympathetic nerves (ETB def) had a greater degree of hypertension in response to a HS diet compared to their male counterparts when measured by the tail cuff method. However, we now report that salt-induced hypertension is not different between sexes when measured by telemetry. Therefore, additional experiments were designed to test the hypothesis that female ETB def rats are more sensitive to acute stress when on a HS diet. The pressor response, measured by telemetry, to acute air jet stress was similar between male transgenic control (Tg control) and ETB def rats following chronic HS intake. In contrast, female ETB def rats had a significantly greater pressor response (about twofold higher) than female or male Tg control or male ETB def rats maintained on HS, a finding that cannot be explained by increased vascular reactivity to ET-1 in female rats as we observed that male ETB def rats had a greater pressor response to i.v. infusion of ET-1 compared to females. Furthermore, HS feeding exacerbated the pressor response to ET-1 in both male and female ETB def rats. Given our previous studies demonstrating that the ETA receptor functions to reduce the pressor response to acute stress, these findings further support a role for the ET receptor system in the pressor response to acute stress and that female rats have reduced ETA receptor activity when on a HS diet compared to males.

Blood Pressure Management in Acute Stroke

Whether raised blood pressure in patients with acute stroke should be treated is one of the major unresolved issues in acute stroke management, due mainly to a paucity of reliable data from sufficiently powered randomized controlled trials. However, the Scandinavian Candesartan Acute Stroke Trial (SCAST), recently published in The Lancet , adds important new information about the risks and benefits of treatment of poststroke hypertension.1 Else Sandset and colleagues assessed whether careful blood pressure-lowering treatment with candesartan is beneficial in a wide range of patients with acute ischemic and hemorrhagic stroke and raised blood pressure. ### Rationale for Blood Pressure-Lowering in Acute Stroke Blood pressure is increased in up to 75% to 80% of patients with acute stroke and usually decreases spontaneously over the next few days.2–4 The cause of this transient rise in blood pressure (ie, poststroke hypertension) is unknown. A specific physiological reaction to the stroke itself is often postulated, possibly due to disturbed cerebral autoregulation,5 damage or compression of brain regions that regulate the autonomic nervous system,6 or neuroendocrine factors.7,8 However, nonstroke-specific mechanisms such as headache,6 urine retention,6 infection,9 and psychological stress of admission to hospital10,11 have also been postulated. Data from observational studies have consistently shown that raised blood pressure after stroke is associated with poor short- and long-term outcomes.12–14 In patients with acute ischemic stroke, raised blood pressure is potentially harmful because it increases the risk of cerebral edema and hemorrhagic transformation in the freshly infarcted brain tissue.6 In patients with hemorrhagic stroke, high blood pressure increases the risk of hematoma expansion, growth of the perihematomal edema, and early rebleeding into the brain.15 However, optimum management of poststroke hypertension remains controversial, particularly in ischemic stroke, in which there are concerns that lowering blood …

Transient Increases In Blood Pressure After Spontaneous Bursts Of Muscle Sympathetic Nerve Activity: Contributions Of Cardiac Output And Systemic Vascular Conductance

Previously, a latency of 5.5 seconds between the occurrence of a burst of muscle sympathetic nerve activity (MSNA) and the subsequent peak arterial blood pressure (BP) response was reported. Although this BP increase was thought to be primarily due to peripheral vasoconstriction, beat-to-beat vascular conductance measures were not made. Furthermore, a transient cardio-acceleration was observed following MSNA bursts. However, whether an increase in cardiac output contributes to the BP response is unknown. PURPOSE: To assess the beat-to-beat fluctuations in cardiac output (CO) and systemic vascular conductance (SVC) following a spontaneous burst of MSNA. METHODS: In 7 young men, BP (finger photoplethysmography), stroke volume (SV; Modelflow), heart rate (HR; ECG) and MSNA (microneurography) were continuously measured during 30 minutes of supine rest. Beat-to-beat fluctuations in BP, CO (HR × SV) and systemic vascular conductance (SVC; CO/MAP) were characterized for 15 cardiac cycles following each individual MSNA burst using signal averaging to identify the temporal pattern for each variable and a peak response was calculated. RESULTS: A significant rise in diastolic BP was observed following each burst of MSNA with a peak increase of 4.35 ± 0.5 mmHg (+6.6 ± 0.7%; p<0.05) occurring at a latency of 5.4 ± 0.2 s. Within the first 2 cardiac cycles following an MSNA burst, the immediate (1.7 ± 0.05 s) increase in BP was associated with a 0.49 ± 0.10 L (+10 ± 0.03%; p<0.05) increase in CO. SVC was also transiently increased with CO during this initial period but then subsequently decreased by -0.005 ml·min-1mmHg-1 (-8.1 ± 0.4%; p<0.05), reaching a maximum reduction around the time of the peak increase in BP. CONCLUSIONS: These preliminary findings indicate that spontaneous bursts of MSNA consistently produce elevations in BP that appear to be mediated by alterations in both CO and SVC. The initial rise in BP is associated with an increase in CO that transitions to peripheral vasoconstriction, noted by the significant fall in SVC at the time of the peak BP response. Thus, it appears that both central and peripheral adjustments contribute to the transient rise in BP following a spontaneous burst of MSNA.

Regular Khat (Catha edulis) chewing is associated with elevated diastolic blood pressure among adults in Butajira, Ethiopia: A comparative study

BackgroundFresh leaves and buds of the Khat plant (Catha edulis) contain Cathinone, an amphetamine like alkaloid responsible for its pharmacological action. Chewing of Khat has been associated with a transient rise in blood pressure and heart rate in experimental studies. Few studies examined the effect of regular or frequent Khat chewing on blood pressure at the population level. This study was conducted to examine the association of regular Khat chewing with blood pressure among adults.MethodsWe compared systolic and diastolic blood pressure of adults 35-65 years of age who reported regular chewing of Khat during the preceding five years to those who never chewed Khat during the same period. Study participants were recruited from purposively selected urban and rural villages of Butajira District in Ethiopia. The comparative groups, chewers (334) and non-chewers (330), were identified from among the general population through a house-to-house visit using a screening questionnaire. They were frequency-matched for sex and age within a five-year range. Data were collected through structured interviews and physical measurements including blood pressure, weight and height.ResultsThe prevalence of hypertension was significantly higher among Khat chewers (13.4%) than non-chewers (10.7%), odds ratio (OR) = 1.66 (95% confidence interval (CI) 1.05, 3.13). A considerably high proportion of chewers (29.9%) than non-chewers (20.6%) had sub-optimal diastolic blood pressure (> 80 mmHg). The mean (sd) diastolic blood pressure was significantly higher among Khat chewers [75.0 (11.6)] than non-chewers [72.9 (11.7)], P < 0.05. Similarly, Khat chewers had significantly higher mean (sd) heart rate [76.3 (11.5)] than non-chewers [73.9 (12.6)], P < 0.05. There was no significant difference in mean systolic blood pressure between the two groups.ConclusionRegular chewing of Khat is associated with elevated mean diastolic blood pressure, which is consistent with the peripheral vasoconstrictor effect of Cathinone. Regular Khat chewing may have sustained effects on the cardiovascular system that can contribute to elevated blood pressure at the population level.

Blood pressure lowering in acute ischaemic stroke: an update on the role of angiotensin receptor blockers

Blood pressure lowering in acute ischaemic stroke: an update on the role of angiotensin receptor blockers

Is there an association between severe job strain, transient rise in blood pressure and increased mortality?

Background. Job strain may be associated with various diseases and increased mortality but there is little data available from prospective studies with long‐term follow‐up. Objective. To assess the effect of heat exposure followed by severe job strain on blood pressure, heart rate and mortality. Design. Prospective 19‐year observational study (1982–2000) of a cohort of employees in a ferry alloy plant undergoing two economical crises. The participants were 218 healthy males aged 30–59 years. Measurements. Annual standardized measurements of blood pressure, heart rate, serum cholesterol and registration of morbidity and mortality. Results. Heat‐exposed men (n = 25) and non‐heat‐exposed men (n = 193) had unchanged blood pressure from 1982 to 1984. Thereafter the plant underwent two serious economic crises, in 1985–87 and 1990–91, respectively. The first one was handled by decisions exclusively taken by the head office and included a gradual lay‐off of 25% of the workers, and the second one was handled jointly between the local management, union leaders and employees and included a modest, voluntary lay‐off. Thus, the two crises differed markedly in low vs high job control. Blood pressures gradually increased from 1985 to 1988 in the whole cohort until systolic blood pressure reached 15 mmHg and diastolic blood pressure 12 mmHg above baseline levels (p<0.001). Thereafter blood pressures decreased to slightly above baseline levels and then remained unchanged for the next 5 years. However, heart rate increased from 62±12 beats/min in 1982–83 to 69±10 beats/min in 1988 (p<0.01) and did not return to baseline. Total mortality by 31 December 2000 in the study cohort was significantly higher over the 19 years of follow‐up than among age‐matched, Norwegian men (p<0.01). Conclusions. If a cause–effect relationship exists between the first economical crisis in the ferry alloy plant and the concomitant rise in blood pressure, job strain had a powerful but time‐limited effect on blood pressure. Since the same phenomenon was not reproduced 5 years later, the marked difference in job control (high vs low) may constitute the difference. Alternatively, age‐related effects or adaptive coping mechanisms may have prevented a similar second blood pressure rise despite exposure to a job strain of similar severity. However, there was also a high 19‐year total mortality in the study population, which could be related to long‐term health consequences of the first or both economic crises. This study provides some support for the notion that increased job strain elevates blood pressure and deteriorates outcome.

The cardiovascular and behavioral response to cat odor in rats: unconditioned and conditioned effects

Cardiovascular and behavioral responses were recorded in rats during exposure to cat odor. Rats were habituated to an open rectangular arena that contained a small enclosed wooden box in which they could hide. On day 1 of the experiment, after 30 min in the apparatus, rats were presented with a piece of fabric collar for 60 min. On day 2, rats were presented with an identical piece of fabric collar, except that it had been worn by a cat and therefore exuded cat odor. On day 3, rats were again presented with an unworn cat collar, to determine any conditioned responses to the environment or stimulus (collar) previously associated with cat odor. Results showed significantly increased blood pressure and decreased activity during exposure to cat odor as well as avoidance of the odor stimulus and an increase in vigilance and risk-assessment measures. No significant change in heart rate was found during cat odor exposure. On day 3, a transient increase in blood pressure was seen as well as reduced activity and a range of defensive behaviors. This suggests some conditioning of fear to a context in which cat odor had previously been experienced. Heart rate was also significantly decreased on day 3. A transient rise in blood pressure was also seen when the unworn cat collar was placed into the apparatus on day 3, suggesting a conditioned response to a stimulus that has been previously associated with cat odor. This study demonstrates that a natural stressful stimulus can induce both unconditioned and conditioned autonomic and behavioral responses.

Grading of cerebral autoregulation in preterm and term neonates

The response of cerebral blood flow velocity to a single spontaneous transient rise in blood pressure was studied to grade the cerebral autoregulatory response of newborns. Blood pressure was measured continuously through an umbilical or peripheral arterial catheter; continuous flow velocity recordings were taken from the middle cerebral artery using continuous wave Doppler ultrasound. From a cohort of 62 healthy term and preterm neonates, 325 transients in mean arterial blood pressure and mean cerebral blood flow velocity were identified for analysis using a foot-seeking algorithm. An initial classification of active or impaired autoregulation was given to each transient using a self-clustering technique. The grading of the transients was studied by examining the slope of the return of the cerebral blood flow velocity to baseline. Negative slopes indicate a normal autoregulation; slopes of 0 or greater indicate an absence of autoregulation. This classification was in agreement with the self-clustering method (Cohen’s kappa = 0.94, P < 0.0001). The relationship between the autoregulatory response assessed by the grading method and gestational age, postnatal age, and P co 2 was examined using linear regression analysis. A significant relationship with gestational age ( P = 0.002) but not P co 2 ( P = 0.06) or postnatal age ( P = 0.14) was evident.

Plasma catecholamines in pre- and in postmenopausal women with mild to moderate essential hypertension

The sympathetic nervous system (SNS) is thought to play an important role in the pathogenesis of essential hypertension and many studies have established a relationship between plasma levels of norepinephrine (NE) and epinephrine (E) and sympathetic nervous activity (SNA). Furthermore, it has been suggested that climacteric women are more exposed to psychosocial stress which can produce a transient rise in blood pressure (BP) and, with time, determine a hypertensive state. Plasma NE and E levels were measured at rest and after physiological stimulation (head-up tilt test) in 20 hypertensive (BP: 146 +/- 13/101 +/- 4 mm Hg) and in 20 normotensive women (BP: 132 +/- 7/85 +/- 4 mm Hg). Women in each of these two groups were further subdivided according to their climacteric status (10 premenopausal and 10 postmenopausal women). No difference in NE values at rest was found between groups and subgroups. During head-up tilt test, Ln NE plasma values increased in normotensive and hypertensive groups; the rise was significantly higher in hypertensive than in normotensive women (P < 0.01). In climacteric subgroups, Ln NE appeared markedly increased above resting levels in pre- and postmenopausal hypertensive women when their position was changed from supine to upright (P < 0.01). Since high plasma NE levels after stimulation (head-up tilt) are associated with sympathetic overactivity, we conclude that SNA is involved in the pathogenesis of essential hypertension in climacteric women.

Hypertension and stroke.

In acute stroke, a transient rise in blood pressure is common, in some cases superimposed on chronic hypertension. No major controlled trials have reported findings on whether blood pressure should be lowered acutely in such patients. On the basis of observational studies and haemodynamic considerations, it seems prudent to leave all but the highest blood pressures in acute stroke to settle spontaneously. ISCHAEMIC STROKE: Ischaemic stroke may occasionally be precipitated by overzealous blood pressure reduction. This has been reported in particular in the initial treatment of very severe hypertension, and occasionally in the elderly hypertensive. It may also occur in the rare cases where transient cerebral ischaemia is haemodynamically induced.

Inhibition of supraoptic vasopressin neurones following systemic clonidine.

Experiments were undertaken in urethane-anaesthetized rats to investigate the effects of systemic clonidine on the firing of supraoptic vasopressin (VP) neurones, which were identified by their characteristic phasic activity pattern. Injection of clonidine (50 micrograms/kg i.v.) reduced the firing of all 16 VP neurones tested, and their overall mean activity decreased from 5.09 +/- 1.01 to 1.63 +/- 0.64 spikes/second (P < 0.02). In VP cells which were already firing phasically before clonidine, the inhibition resulted in complete quiescence. In VP cells which were originally continuously active, the inhibition resulted in a switch to phasic activity. This inhibitory effect, which was prevented by prior injection of the alpha-2 antagonist idazoxan (0.5 mg/kg), had a mean duration of 11.8 +/- 1.8 min. Subsequent experiments revealed that i.v. clonidine (50 micrograms/kg) caused a transient rise in blood pressure, but this had a shorter time-course and was unlikely to account for the prolonged neuronal inhibition. It was concluded that systemic clonidine acts centrally to suppress the activity of hypothalamic VP neurones, thereby explaining the fall in plasma VP levels found in previous studies.

Stroke and Antihypertensive Therapy

Antihypertensive treatment effectively prevents haemorrhagic and lacunar stroke, and apparently also transient ischaemic attacks. It is likely that treatment also affords some protection against other thrombotic strokes. Acute stroke is often associated with a transient rise in blood pressure, which may be superimposed on a chronic hypertensive state. Emergency treatment of hypertension should probably only be given to the most extremely elevated pressures in acute stroke. In the occasional patient, overzealous antihypertensive treatment may cause cerebral ischaemia or even ischaemic stroke. Aside from acute stroke with transient hypertension, the risk of overtreatment is most marked in very severe hypertension, in the frail elderly hypertensive with postural hypertension, and in the rare cases of haemodynamically mediated transient ischaemic attacks. (Hypertens Res 1994; 17 Suppl. I: S59-S61)

Identification of sleep disruption and sleep disordered breathing from the systolic blood pressure profile.

Respiratory sleep studies are frequently performed to identify sleep disruption resulting from upper airway obstruction. Traditional polysomnographic studies may not detect brief recurrent sleep disruption and thus fail to recognise a significant problem when apnoea, hypopnoea, or arterial desaturation are not present. Arousal from sleep causes a transient blood pressure rise, and each inspiration causes a transient blood pressure fall. This study assesses whether these blood pressure changes are a useful indirect marker of disturbed sleep, obstructed sleep apnoea, and snoring related sleep disturbance. Computer algorithms were developed to identify blood pressure falls caused by inspiration and rises related to arousal from 286 sleeping blood pressure samples of a consistent respiratory state drawn from 51 polysomnographic studies. From these samples, normal ranges for the number of arousal related systolic rises and the average size of the inspiratory falls were established. These were then applied prospectively to all night unedited blood pressure recordings from a further 20 subjects. The size of the inspiratory falls in blood pressure progressively increased from normal sleep, through snoring, to frank obstructive sleep apnoea. The 95th centile of normal was 12.5 mm Hg. The number of arousal related blood pressure rises also increased during obstructive sleep apnoea and periods of snoring with associated arousals, compared with normal undisturbed sleep, and all these periods of disturbed sleep included more than 30 such rises per hour. When these blood pressure features were examined in the 20 subjects studied prospectively, the six with a sleep related breathing disorder could all have been identified from their systolic blood pressure profile alone. The systolic blood pressure profile may be helpful in identifying patients with obstructive sleep apnoea, snoring with arousals, or other sleep disruption syndromes.

The Development of Hypertension in Rats with Intraventricular Grafts of Fetal SHR or WKY Hypothalamus

To evaluate the role of the hypothalamus in hypertension, we compared the. development of blood pressure (BP) in normotensive host rats grafted at weaning with fetal hypothalamus from genetically hypertensive or normotensive donors. The anteroventral region of the third ventricle (AV3V) has been implicated in the control of BP, such that lesions of AV3V prevent or attenuate hypertension in a number of animal models. Recent studies have shown that BP is elevated after grafting SHR hypothalamus into the AV3V region of genetically normotensive hosts. WKY hosts grafted with fetal SHR hypothalamus (E15) exhibited increased BP for over 5 months after implantation, while hosts receiving WKY hypothalamus experienced only a transient rise in BP at 1 month post-implant /1/. Normal Wistar hosts grafted with older (E19-20) SHR hypothalamus exhibited increased BP at 1 month post-implant, and not at subsequent ages, while E19-20 WKY hypothalamus did not influence BP at any age /2/. The following experiments were designed to determine how the pressor effects of grafting SHR hypothalamus may vary as a function of the embryonic age and specific anatomical origin of grafted cells. Two normotensive rat strains were used as hosts: outbred Wistar and inbred Wistar-Kyoto (WKY) rats. At 25 days of age, hosts were grafted in the AV3V region with E15-16 fetal SHR hypothalamus, SHR cortex or WKY hypothalamus. Sham-operated controls received infusions of 0.9% saline. Systolic blood pressure was measured at 30, 60, 90 and 120 days of age. Based on evidence that the AV3V region also mediates behavioral control of fluid/electrolyte homeostasis, daily consumption of water and 1.5% saline was also measured at 60 and at 120 days of age.

The Effect of Caffeine on Daytime Ambulatory Blood Pressure

Caffeine produces an acute increase in blood pressure in the research laboratory, but its effect on the ambulatory blood pressure during normal daily activities is unknown. In 25 normotensive, caffeine-naive subjects, daily administration of 400 mg caffeine produced a small increase (+3/+3 mm Hg, P less than .001) in ambulatory daytime blood pressure on the first day, with values returning to baseline by the third day. The initial rise in blood pressure was associated with a fall in heart rate (-3 beats/min, P less than .02). Readings taken the morning following the first day of caffeine ingestion did not show any persistent effect of caffeine on blood pressure. A 400 mg dose of caffeine causes a small increase in daytime ambulatory blood pressure, but tolerance develops with daily caffeine consumption. Infrequent ingestion of caffeine may cause a transient rise in blood pressure which is unlikely to be harmful to an individual but might influence the diagnosis of hypertension in a patient with a borderline elevated blood pressure.

Pressor effects following microinjection of 5‐HT1A receptor agonists into the raphe obscurus of the anaesthetized rat

1. The effects of electrical stimulation and microinjections (90 nl) of the 5-HT1A receptor agonists, flesinoxan and 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT), and glutamate into the raphe obscurus on blood pressure, heart rate and phrenic nerve activity (central inspiratory drive) were investigated in rats anaesthetized with alpha-chloralose. 2. Electrical stimulation of the raphe obscurus caused a rise in blood pressure which was associated with bradycardia, while glutamate (2.7 nmol) caused only a rise in blood pressure. 3. Flesinoxan (1.3 nmol) and 8-OH-DPAT (0.7 nmol) increased blood pressure by 9 +/- 1 and 14 +/- 2 mmHg, respectively and did not affect heart rate. For both agonists the effect on blood pressure was shown to be dose-dependent; again no effect on the heart rate was observed over the dose-ranges chosen. 4. Microinjections of the non-selective 5-HT1A receptor antagonists, (+/-)-pindolol (2.7 nmol) or methiothepin (5.2 nmol), into the raphe obscurus prevented the increase in blood pressure caused by microinjection of flesinoxan. However, (+/-)-pindolol caused a sustained rise in blood pressure of 15 +/- 1 mmHg while methiothepin caused a transient rise in blood pressure. Neither drugs affected heart rate. The ability of methiothepin to attenuate the pressor effect of flesinoxan was found to be partially reversed after 30 min. 5. It is suggested that activation of 5-HT1A receptors within the raphe obscurus can cause sympatho-excitation.

C5a/C5ades-Arg-induced increase in blood pressure in the guinea pig: role of thromboxane

Cleavage of the complement protein C5 by activation of the complement system yields a low molecular weight fragment C5a. Knowledge of the alterations in blood pressure induced by C5a as well as the mediators responsible for the blood pressure changes may provide information concerning the potential role of C5a in the adverse hemodynamic responses associated with complement activation. The purpose of this study was to characterize changes in mean arterial pressure in the guinea pig after intravenous challenge with a combination of guinea pig C5a plus C5ades-Arg(C5a/C5ades-Arg) and determine the mediators responsible for the transient increase in blood pressure which was observed. Mean arterial pressure was monitored in mechanically ventilated pentobarbital-anesthetized guinea pigs. Intravenous injection of C5a/C5ades-Arg consistently caused a marked but transient rise in blood pressure. A transient hypotensive response was also seen with injection of markedly higher doses of guinea pig C5a/C5ades-Arg. Various pharmacological antagonists were used to determine the mediators responsible for the increase in blood pressure induced by guinea pig C5a/C5ades-Arg. We found that the LTD4 antagonist L-649,923 did not inhibit the transient rise in blood pressure. However, the cyclooxygenase inhibitor indomethacin inhibited the C5a/C5ades-Arg-induced pressor response as did the thromboxane synthetase inhibitor U-63557A and the thromboxane receptor antagonist SQ 29,548. In addition, the C5a/C5ades-Arg-induced pressor response was not inhibited by the H1 antagonist pyrilamine, but was inhibited in part by the α-adrenergic antagonist phentolamine. Also, the response was reduced in animals depleted of circulating platelets or white blood cells. Thus, the results of our studies suggest that intravenously injected guinea pig C5a/C5ades-Arg causes release of the vasoconstrictor thromboxane, most likely from circulating white blood cells or platelets, resulting in a transient rise in blood pressure in the guinea pig. In addition, release of catecholamines may contribute to the pressor response observed.