Increments In Arterial Pressure Research Articles

Increment in Systolic Blood Pressure During Cold Pressure Test Is Associated with Baseline LF Power in Young Prehypertensive Men

The cold pressor test (CPT) is commonly used as a sympathoexcitatory maneuver to provoke an increment in arterial pressure and heart rate and to measure cardiovascular reactivity to stress. However, use of the CPT as a predictor test of future hypertension is still debatable. We investigated whether exaggerated blood pressure responsiveness to CPT is observed in young prehypertensive men and determined baseline HRV indices and autonomic nervous system contribution into the elevation of blood pressure.CPT was performed in 81 normotensive and 72 prehypertensive men enrolled from V.N. Karazin Kharkiv National University student population. All participants gave written informed consent. After 5 min resting stage subjects placed their right hand into ice‐cold water for 1 minute. ECG was continuously recorded and resting HRV indices were interpreted (CardioLab 2010). Blood pressure was measured at the end of each stage (Nissei WS‐1011). GLM one‐way MANOVA and MANCOVA with height and BMI were used to test for possible effects of prehypertension on heart rate (ΔHR) and blood pressure (ΔSBP and ΔDBP) responses. The stepwise multiple linear regression analysis was carried out to assess the relative importance of baseline LnLF (LnLFrest) and LnHF (LnHFrest) power in HR, SBP, and DBP increments, adjusted also for the presence of prehypertension, BMI, height, and two‐way interactions.In the current study, prehypertensive subjects did not demonstrate higher cardiovascular reactivity to CPT (Table 1). Moreover, normotensives had higher SBP response to CPT (Table 1). When height and BMI were taken into account this difference was even more significant (not shown). Previous studies have yielded inconsistent results with some showing higher and some showing the same and even lower blood pressure reactivity to CPT in prehypertensive subjects or in persons with family history of hypertension.The stepwise multiple regression analysis revealed that ΔSBP in prehypertensives and ΔDBP in all subjects were negatively associated with LnLFrest possibly indicating, according to our hypothesis, activity of the inhibitory interneurons projected to the presympathetic neurons in the rostral ventrolateral medulla. The central inhibition of sympathetic activity reduced the increment of SBP in subjects developing hypertension and controlled increment of DBP in all subjects (Table 2).It was shown that increments in both SBP and DBP were associated with ΔHR only in the prehypertensive subjects and in persons with increased BMI (Table 2). These findings may be partially explained by blunting of baroreceptor reflex sensitivity and/or resetting of the baroreceptor reflex to a higher control point.in prehypertensives and in subjects with increased BMI. The increments in SBP and DBP associated also with ΔHR in subjects with a high level of baseline parasympathetic activity as shown by the positive association between LnHFrest by ΔHR interaction and ΔSBP or ΔDBP (Table 2) possibly because high LnHFrest reduces HR and increases atrioventricular delay which may contribute to a ventricular filling.In conclusion, young prehypertensive subjects demonstrated lower SBP response to CPT than normotensives possibly due to their increment in SBP was associated with resting LnLF power, indicating according to our hypothesis, inhibition of the presympathetic medullary neurons; ΔSBP and ΔDBP were associated with ΔHR only in prehypertensives and in persons with high baseline parasympathetic activity.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Role of angiotensin II in arterial pressure and renal hemodynamics in rats with altered renal development: age- and sex-dependent differences

Numerous studies have demonstrated that angiotensin II (ANG II) is involved in hypertension and renal changes occurring as a consequence of an adverse event during renal development. However, it was unknown whether this involvement is sex and age dependent. This study examines whether the increments in arterial pressure (AP) and in the renal sensitivity to ANG II are sex and age dependent in rats with altered renal development. It also evaluates whether the ANG II effects are accompanied by increments in AT(1) receptors and oxidative stress. Experiments were performed in 3- to 4- and 10- to 11-mo-old rats treated with vehicle or an AT(1) receptor antagonist (ARAnp) during the nephrogenic period. ARAnp-treated rats were hypertensive, but an age-dependent rise in AP was only found in males. Three days of treatment with candesartan (7 mg·kg(-1)·day(-1)) led to a fall of AP that was greater (P < 0.05) in male than in female 10- to 11-mo-old ARAnp-treated rats. Oxidated proteins were elevated (P < 0.05), and the decrease in AP elicited by candesartan was reduced (P < 0.05) when these rats are also treated with tempol (18 mg·kg(-1)·day(-1)). Hypertension was not maintained by an elevation of AT(1) receptors in kidneys and mesenteric arteries. The acute renal hemodynamic response to ANG II (30 ng·kg(-1)·min(-1)) was similarly enhanced (P < 0.05) in both sexes of ARAnp-treated rats at 3-4 but not at 10-11 mo of age. Our results suggest that an adverse event during the nephrogenic period induces an ANG II-dependent increment in AP that is aggravated only in males during aging and that oxidative stress but not an increase in AT(1) receptor contributes to the rise in AP. This study also shows that the renal hemodynamic sensitivity to ANG II is transitorily enhanced in both sexes of rats with altered renal development.

Miscellaneous Item

CardioOascular Research introduced a Cardiovascular w x Mystery Series several years ago 1 . Included amongst its Ž . objectives: a an exploration of less well known aspects of Ž . cardiovascular disease; b an integration of basic and Ž . clinical sciences and c an intention to be provocative. A clinical vignette, in the form of a mystery story, sets the stage for an invited mini-review on a topic that addresses these objectives. As Series Editor, I was delighted when Professor of Pathology, William E. Stehbens, found the w x vignette ‘Vascular aneurysms: a side-splitting affair’ 2 and its patients M. and F. sufficiently provocative to bring forward his views in a Letter to the Editor entitled ‘The pathogenesis of arterial aneurysms and associated lesions’. Drawing on traditional concepts, Stehbens has emphasized the importance of ‘hemodynamic biomechanical stress’ in promoting such iterations in vascular architecture. He indicates ‘‘...aneurysms develop when intravascular pressure is greater than the wall can withstand...’’ and ‘‘...aneurysms indicate mural weakness’’. I completely concur with the latter—an intrinsic defect in the tensile strength of the vessel wall is responsible for its aneurysmal dilatation—and would add that such loss of vascular integrity is not based on prevailing andror repetitive surges in intraluminal pressure. Hypertension is not a prerequisite; it does predispose to aneurysmal dilatation in a weakened vessel. Aneurysms complicate many different diseases and clearly do not have a single pathogenic origin. Potential causes include abnormal structural protein phenotype and proteinase-mediated degradation of such proteins as collagen and elastin. One would not confuse the pathogenesis of aneurysmal dilatation seen in inherited connective tissue Ž . disorders e.g., Marfan’s syndrome with that associated with acquired atherosclerotic disease. In the mini-review w x that follows the vignette 3 , Herron provides a compelling argument for the involvement of matrix metalloproteinases in the formation of abdominal aortic aneurysm. Stehbens goes on to discuss patient M. with adult dominant polycystic kidney disease and correctly indicates that it is unknown whether proteinase activity is increased in the aneurysms of the cerebral circulation that appear in this entity. This is also true for abdominal aortic aneurysm, dissecting aneurysm of the thoracic aorta, mitral valve prolapse and intestinal diverticula associated with this inherited disorder. There likewise is no documented evidence for abnormal structural protein phenotype in this entity. However, does it not seem likely that either scenario would explain this unusual predisposition to ‘weakness’ in these diverse tissues whose fibrillar type I collaw x gen should have the tensile strength of steel 4 ? Weightlifters experience sudden and marked increments in arterial pressure during isometric exercise, but they experience neither mitral valve prolapse nor arterial aneurysm. Aneurysmal formation appears subsequent to emboli of myxomatous tissue as was the case in patient F. In contrast to septic or bland emboli, such tumor emboli contain pluripotent cells, such as the myofibroblast phenotype w x 5,6 . These cells can express proteinases that account for their ability to invade vascular tissue with destruction of w x elastic lamina and media 7,8 . These emboli resemble the metastatic behavior of neoplastic tissue, where proteinase w x activation is an integral feature 9 . Even after removal of the tumor embolus, the continued presence of such cells within the invaded vessel leads to its destruction with w x subsequent aneurysmal formation 10 . In closing, a localized defect in tissue tensile strength leads to its distention. This is expressed as aneurysmal dilatation in the case of blood vessels, diverticula of the intestine and prolapse of valve leaflets. To implicate hypertension, a hemodynamic condition present throughout the arterial vasculature and left ventricular chamber, as the predominant causal mechanism for localized tissue weakness is no longer tenable and unwarranted, in my opinion. We are what we know and we see what we want according

Acute and chronic cyclooxygenase blockage in portal-hypertensive rats: Influence in nitric oxide biosynthesis

BACKGROUND & AIMS: Prostacyclin and nitric oxide have been involved in the hyperkinetic syndrome in portal hypertension. The aim of this study was to investigate the relative contribution and possible interaction between prostacyclin and NO in this circulatory abnormality. METHODS: Portal vein-ligated and sham-operated rats received indomethacin and vehicle either on a short-term (5 mg/kg subcutaneously) or long-term basis (5 mk.kg-1.day-1, continuous 7-day infusion with an osmotic minipump). Measurements of arterial pressure and superior mesenteric arterial flow (mL.min-1.kg-1, ultrasonic flow probe) were then performed before and after NG-nitro-L-arginine methyl ester (L-NAME) injection (13 mg/kg intravenously). RESULTS: Short-term or long-term indomethacin treatment had no effect in sham-operated rats but significantly decreased mesenteric arterial flow in portal-hypertensive rats. Mesenteric flow remained higher after long-term than after short- term indomethacin treatment (54.5 +/- 2 vs. 46.1 +/- 2; P = 0.01). This blunted response to long-term indomethacin treatment was associated with an enhanced response to L-NAME, shown by greater increments in arterial pressure (29% +/- 3%) and mesenteric arterial resistance (209 +/- 22%) in indomethacin-treated rats than in rats receiving vehicle (19% +/- 2% and 130% +/- 20%; P < 0.05). CONCLUSIONS: Both prostacyclin and NO contributed to splanchnic hyperemia in portal-hypertensive rats. There was an enhanced release of NO after long-term prostacyclin inhibition, suggesting that both vasodilatory systems interact, promoting splanchnic hyperemia in portal hypertension. (Gastroenterology 1996 May;110(5):1529-35)

Nitric Oxide and Renal Regulation of Sodium Excretion

The importance of nitric oxide in the acute and long-term regulation of arterial pressure and renal function is supported by the results obtained in many studies. Reports described in this brief review provide evidences that nitric oxide plays an important role in regulating the urinary sodium and water excretion in basal conditions and during increments in arterial pressure and extracellular volume. Data showing an important interaction between nitric oxide and angiotensin II or prostaglandins in the regulation of the renal excretory function is also provided. These studies support the concept that the development of sodium sensitive hypertension could be secondary to a deficient nitric oxide production.

Vasopressin receptors in the area postrema differentially modulate baroreceptor responses in rats

This study examined the effects of microinjection of [Arg 8]vasopressin (AVP) into the area postrema (AP) on baroreceptor reflex control of heart rate (HR) and sympathetic efferent discharge (SED) in anesthetized rats. Comparable increments in blood pressure evoked by systemic AVP, as opposed to phenylephrine, were associated with significantly greater reflex bradycardia. Similarly, AVP augmented the baroreflex-mediated sympathoinhibition; however, this effect was evident only with the lower increments in arterial pressure (< 45 mm Hg) i.e. following systemic administration of small doses of AVP. Beyond 45 mm Hg there was no further augmentation of baroreflex-mediated sympathoinhibition showing the non-linearity of the response compared to phenylephrine which was linear over a wide range of induced pressure increases. Microinjection of AVP into the AP produced a differential effect on HR and SED responses to baroreceptor activation by systemically administered phenylephrine, the baroreflex slope of HR response was attenuated whereas that of SED was enhanced. Microinjection of the V 1 antagonist AVPX (d(CH 2)5Tyr(Me)-AVP) into the AP abolished the inhibitory effect of AVP on the baroreceptor-HR response suggesting that V, receptors are involved in this response. Further, AVPX inhibited the baroreceptor-SED response suggesting that V, receptors in the AP are tonically involved in modulating the baroreceptor reflex control of SED. Qualitatively similar but smaller responses were obtained following microinjection of AVP into the nucleus tractus solitarii (NTS) suggesting involvement of neural input from the AP to the NTS in AVP-evoked responses in the AP. It is concluded that the AVP receptors in the AP differentially modulates the baroreceptor reflex control of HR and SED.

Changes in CSF pressures during experimental acute arterial subdural bleeding in pig.

The effects of acute arterial subdural bleeding on cerebrospinal fluid (CSF) pressure and 12 other vital parameters were studied in spontaneously breathing pigs (group 1, n = 9) and in mechanically ventilated pigs (group 2, n = 18) to analyze quantitatively the bleeding course and the lethal mechanism. Spontaneously breathing animals all succumbed after a mean bleeding volume of 45.6 +/- 8.9 ml, corresponding to about 50 per cent of the intracranial volume, and a mean bleeding duration of 11.0 +/- 2.6 min. Rapid rise in CSF pressures, marked transtentorial pressure gradients, and progressive reductions of cerebral perfusion pressure leading to a permanently iso-electric EEG, apnoea and to a terminal rise in arterial pressure (Cushing response), was the rule in these animals. The mechanically ventilated animals had smaller bleeding volumes (34.3 +/- 8.1 ml), but longer bleeding durations (13.8 +/- 5.8 min). In this group 7 animals survived. They had no pressure gradients, and only moderate changes in arterial pressure and EEG. The 11 animals that succumbed had marked transtentorial pressure gradients, but smaller increments in arterial pressure than the spontaneously breathing animals. At autopsy, subdurally located blood was found throughout the intracranial and spinal subdural compartments and along the spinal nerve roots in both groups. The results of this study suggest that survival after acute subdural haematoma is influenced by the presence of transtentorial pressure gradients and by the spinal sac acting as a space for expansion. The beneficial effect of artificial ventilation is discussed.

Angiotensin II attenuates baroreflex control of heart rate and sympathetic activity.

We determined whether angiotensin II (ANG II) modulates the arterial baroreflex control of lumbar sympathetic nerve activity (LSNA) in chloralose-anesthetized rabbits. Intravenous infusion (iv) of ANG II caused significantly less reflex bradycardia and less inhibition of LSNA than iv phenylephrine (PE) for equivalent increments in arterial pressure. During a background iv infusion of ANG II, which caused a small sustained increase in arterial pressure, the reflex inhibition of heart rate (HR) and LSNA in response to further increases in pressure with graded doses of PE was attenuated, but the reflex increase in HR and LSNA in response to hypotension with graded doses of nitroprusside was unchanged. This modulation of the baroreflex by ANG II is specific since a similar background infusion of PE did not alter baroreflex responses to further increases or to decreases in arterial pressure. The frequency of aortic baroreceptors was comparable for equivalent increases in pressure caused by iv ANG II or PE. When ANG II was confined to the isolated carotid sinuses, the reflex inhibition of HR and LSNA during distension of carotid sinuses was unchanged. An excitatory effect of ANG II on the efferent limb of the baroreflex that would oppose the reflex bradycardia or inhibition of LSNA is unlikely because when the pressor effect of ANG II was prevented by nitroprusside, there were no changes in HR and LSNA. We conclude that through an effect on the central nervous system iv ANG II has a selective effect on the arterial baroreflex; it impairs reflex decreases in HR and LSNA during hypertension but not reflex increases in HR and LSNA during hypotension.

Sodium-induced elevation of blood pressure in the anephric state.

Normotensive anephric rats infused with 2 milliliters of a hyperosmolar solution of either sodium chloride or mannitol showed an increase in arterial pressure that was very pronounced with the sodium chloride and that could be partly abolished by administration of an antagonist to the vasopressor action of antidiuretic hormone (ADH). Rats with congenital ADH deficiency subjected to the same treatment showed smaller increments in arterial pressure that remained unchanged after administration of the ADH antagonist. Expansion of intravascular fluid volume was similar in all four groups and bore no correlation to the change in arterial pressure. It is concluded that about half of the increase in blood pressure induced by saline was attributable to the vasopressor effect of stimulated ADH and the remainder to an additional sodium-related factor, since it was more pronounced in the saline-infused than in the mannitol-infused groups. Expansion of the intravascular volume per se could only account for a minimal part of the increment in pressure.

Studies on the mechanism of hypernatriuresis in essential hypertension in relation to measurements of plasma renin concentration, body fluid compartments and renal function.

1. In twenty-two patients representing different stages of benign essential hypertension, hyperosmotic saline was administered intravenously. Determinations of intra-arterial pressure, renal plasma flow, glomerular filtration rate and plasma renin concentration were carried out before and, in the majority, also during and after saline infusion. Changes in cardiac output were followed in ten patients. Plasma volume and extracellular volume were determined in the control period only, although haemodilution was assessed by haematocrit readings. 2. Excess of sodium excretion showed a wide range and was related to the patient's age, as well as to a set of parameters reflecting intrarenal pressure patterns; hypernatriuresis consistently occurred in older patients, in whom renal vascular resistance and nitration fraction were elevated and plasma renin was suppressed. It could not be clarified whether hypernatriuresis together with renin suppression were determined by intrarenal pressure relationships or by an independent age-related factor in the hypertensive patient. 3. Excess of sodium excretion was not related to increments in arterial pressure, cardiac output, renal blood flow or glomerular filtration rate. 4. Plasma renin concentration failed to show consistent changes after hyperosmotic saline infusion. 5. It is concluded that natriuresis is not mediated by changes in the activity of the renin-angiotensin system. Hypernatriuresis appears to be a feature of progressive benign hypertension.