scholarly journals PRESSOR SUBSTANCES IN ARTERIAL HYPERTENSION

1950 ◽  
Vol 92 (6) ◽  
pp. 561-570 ◽  
Author(s):  
Norman S. Olsen ◽  
Henry A. Schroeder ◽  

Pherentasin, a material producing a prolonged pressor response in rats, has been procured from the arterial blood of hypertensive patients and purified. Pherentasin is of small molecular size, non-protein in nature, dialyzable, soluble in water and 90 per cent ethanol, and extractable into organic solvents from alkaline solution. It contains an amino group essential to activity, which is probably primary, and also contains an active carbonyl group. It has been found in concentrations up to approximately 20 γ per liter of blood.

2000 ◽  
Vol 99 (6) ◽  
pp. 527-534 ◽  
Author(s):  
Jens H. HENRIKSEN ◽  
Jens J. HOLST ◽  
Søren MØLLER ◽  
Ulrik B. ANDERSEN ◽  
Flemming BENDTSEN ◽  
...  

Leptin, a peptide hormone produced mainly in fat cells, appears to be important for the regulation of metabolism, insulin secretion/sensitivity and body weight. Recently, elevated plasma leptin levels have been reported in patients with arterial hypertension. Because a change in circulating leptin concentrations in such patients could be caused by altered rates of production or disposal, or both, the aim of the present study was to identify regions of leptin overflow into the bloodstream and of leptin extraction. Patients with arterial hypertension (n = 12) and normotensive controls (n = 20) were studied during catheterization with elective blood sampling from different vascular beds (artery, and renal, hepatic, iliac and cubital veins). Plasma leptin was determined by a radioimmunoassay. Patients with hypertension had significantly elevated levels of circulating leptin (12.8 ng/l, compared with 4.1 ng/l in the controls; P < 0.001), and this was also the case when adjusted for body mass index (BMI) [0.435 and 0.167 ng/l per unit BMI (kg/m2) respectively; P < 0.001]. Circulating leptin was directly related to arterial blood pressure (r = 0.38–0.62, P ⩽ 0.05–0.005) and immunoreactive insulin (r = 0.51, P < 0.62), but not to plasma renin activity. A significant renal extraction ratio for leptin was seen in the hypertensive patients, but this was not significantly lower than that in the controls (0.09 compared with 0.16; P = 0.1). The hypertensive patients had a significantly higher hepatic venous/arterial leptin ratio than the controls (1.02 compared with 0.93; P < 0.02), and this ratio was correlated directly with the BMI (r = 0.38, P = 0.05) and immunoreactive insulin (r = 0.43, P < 0.05). In both hypertensive patients and controls there was a significant spillover of leptin into the iliac vein, but not into the cubital vein. In conclusion, the high concentration of circulating leptin in patients with arterial hypertension is probably caused by increased release of leptin from abdominal (especially mesenteric and omental) and gluteal adipose tissue stores, and renal extraction is slightly reduced. Leptin kinetics in arterial hypertension require further investigation.


1997 ◽  
Vol 273 (3) ◽  
pp. R1126-R1131 ◽  
Author(s):  
Y. X. Wang ◽  
J. T. Crofton ◽  
S. L. Bealer ◽  
L. Share

The greater pressor response to vasopressin in male than in nonestrous female rats results from a greater increase in total peripheral resistance in males. The present study was performed to identify the vascular beds that contribute to this difference. Mean arterial blood pressure (MABP) and changes in blood flow in the mesenteric and renal arteries and terminal aorta were measured in conscious male and nonestrous female rats 3 h after surgery. Graded intravenous infusions of vasopressin induced greater increases in MABP and mesenteric vascular resistance and a greater decrease in mesenteric blood flow in males. Vasopressin also increased renal vascular resistance to a greater extent in males. Because renal blood flow remained unchanged, this difference may be due to autoregulation. The vasopressin-induced reduction in blood flow and increased resistance in the hindquarters were moderate and did not differ between sexes. Thus the greater vasoconstrictor response to vasopressin in the mesenteric vascular bed of male than nonestrous females contributed importantly to the sexually dimorphic pressor response to vasopressin in these experiments.


1990 ◽  
Vol 258 (2) ◽  
pp. R325-R331 ◽  
Author(s):  
D. A. Morilak ◽  
G. Drolet ◽  
J. Chalmers

We have examined the influence of endogenous opioids on the basal and reflex control of arterial blood pressure in the pressor region of the rostral ventrolateral medulla (RVLM) of chloralose-anesthetized rabbits. We tested basal effects both in intact animals and after hypotensive hemorrhage. Bilateral administration of the opiod antagonist naloxone (20 nmol, 100 nl) directly into the RVLM induced a gradual and prolonged increase in mean arterial pressure (MAP) (+17 +/- 2 mmHg). This was preceded by a brief and mild depressor effect (-9 +/- 3 mmHg), which was attributable to a transient reduction in excitability immediately after naloxone injection. When naloxone was administered into the RVLM after hemorrhage (20 ml/kg), it improved recovery of MAP relative to saline controls, again producing a gradual, prolonged pressor response (+29 +/- 5 mmHg). The effect of naloxone on a baroreflex in intact animals was only transient, with a brief, nonsignificant attenuation of the reflex depressor response to aortic nerve stimulation. We conclude that endogenous opioids exert a tonic inhibitory influence on RVLM pressor neurons and that this input remains active after hemorrhage. The RVLM may thus be one site for the beneficial effects of naloxone in preventing circulatory decompensation after hemorrhage. In contrast, opioid neurons are not an essential component of baroreflex-mediated sympathoinhibition in the RVLM.


2021 ◽  
pp. 68-70
Author(s):  
Ketan Prajapati ◽  
Sanket Makwana ◽  
M. J. Sonagara

INTRODUCTION:Hypertension is one of the most important risk factors for cardiovascular disease. The incidence of microalbuminuria is more common among hypertensive patients, even in nondiabetic patients. Microalbuminuria is an independent predictor of cardiovascular morbidity and mortality in patients with essential hypertension. Therefore, current guidelines recommend routine screening of microalbuminuria in hypertensive patients to ensure appropriate interventions are initiated early in the disease process before progression to chronic kidney disease and/or renal failure. AIMS & OBJECTIVES:This study is done to estimate the prevalence of microalbuminuria in patients with normoglycemic hypertension and to identify other variables associated with it. MATERIAL & METHODS:In this study, we randomly selected 100 patients with essential hypertension based on inclusion and exclusion criteria. CBC, renal function test, 24-hour urine albumin excretion (UAE), Body mass index (BMI), and arterial blood pressure measurement were done among all selected patients. Data entry was done in Microsoft Ofce Excel and analysis was done using the software package Epi Info (Version 7.1.5) from CDC, Atlanta, U.S.A. OBSERVATIONS & RESULTS: The study was conducted among 100 hypertensive patients out of which 74 were male and 24 were female. Out of 100 patients, microalbuminuria was present in 44 patients. Mean arterial pressure was found high among patients with microalbuminuria than patients without microalbuminuria. The presence of microalbumin in urine was found to increase with the increasing severity of hypertension. Mean body mass index and serum creatinine were found higher in the microalbuminuric group than the normoalbuminuric group. CONCLUSION:The incidence of microalbuminuria is more common among hypertensive patients, even in nondiabetic patients. The presence of microalbuminuria is an independent predictor of cardiovascular morbidity and mortality in patients with essential hypertension. Screening for microalbuminuria is a relatively simple process, should facilitate early vascular disease detection.


1992 ◽  
Vol 68 (4) ◽  
pp. 1027-1045 ◽  
Author(s):  
A. Randich ◽  
C. L. Thurston ◽  
P. S. Ludwig ◽  
J. D. Robertson ◽  
C. Rasmussen

1. Intravenous administration of 1.0 mg/kg of morphine produces inhibition of the nociceptive tail-flick (TF) reflex, hypotension, and bradycardia in the pentobarbital-anesthetized rat. The present experiments examined peripheral, spinal, and supraspinal relays for inhibition of the TF reflex and cardiovascular responses produced by morphine (1.0 mg/kg iv) in the pentobarbital-anesthetized rat using 1) bilateral cervical vagotomy, 2) spinal cold block or mechanical lesions of the dorsolateral funiculi (DLFs), or 3) nonselective local anesthesia or soma-selective lesions of specific CNS regions. Intravenous morphine-induced inhibition of responses of unidentified, ascending, and spinothalamic tract (STT) lumbosacral spinal dorsal horn neurons to noxious heating of the hindpaw were also examined in intact and bilateral cervical vagotomized rats. 2. Bilateral cervical vagotomy significantly attenuated inhibition of the TF reflex and bradycardia produced by intravenous administration of morphine. Bilateral cervical vagogtomy changed the normal depressor response produced by morphine into a sustained pressor response. Inhibition of the TF reflex in intact rats was not due to changes in tail temperature. 3. Spinal cold block significantly attenuated inhibition of the TF reflex, the depressor response, and the bradycardia produced by intravenous administration of morphine. However, bilateral mechanical transections of the DLFs failed to significantly affect either inhibition of the TF reflex or cardiovascular responses produced by this dose of intravenous morphine. 4. Microinjection of either lidocaine or ibotenic acid into the nuclei tracti solitarii (NTS), rostromedial medulla (RMM), or ventrolateral pontine tegmentum (VLPT) attenuated morphine-induced inhibition of the TF reflex. Similar microinjections into either the periaqueductal gray (PAG) or the dorsolateral pons (DLP) failed to affect morphine-induced inhibition of the TF reflex. 5. Microinjection of either lidocaine or ibotenic acid into the NTS, RMM, VLPT, DLP, or rostral ventrolateral medulla (RVLM) attenuated the depressor response produced by morphine, although baseline arterial blood pressure (ABP) was affected by ibotenic acid microinjections in the DLP. In all these cases, the microinjections failed to reveal a sustained pressor response as was observed with bilateral cervical vagotomy. Similar microinjections into the PAG failed to affect the depressor response produced by morphine. 6. The lidocaine and ibotenic acid microinjection treatments also showed that the bradycardic response produced by morphine depends on the integrity of the NTS, RMM, RVLM, and possibly the DLP, but not the PAG or VLPT.(ABSTRACT TRUNCATED AT 400 WORDS)


1993 ◽  
Vol 264 (1) ◽  
pp. R79-R84 ◽  
Author(s):  
J. N. Stinner ◽  
D. L. Ely

The pressor response to normal daily behaviors and acute stress was studied in black racer snakes (Coluber constrictor) at 30 degrees C. In addition, hematological changes during the stress response were assessed. Mean nighttime systemic arterial blood pressure (SABP) in undisturbed snakes was lower than daytime pressure (26 +/- 3 vs. 32 +/- 9 mmHg, P < 0.001). When snakes were fed mice, SABP increased 3.5- to 4-fold and heart rate increased approximately 3-fold above resting values within approximately 30 s (peak SABP, 99 +/- 18 mmHg; peak heart rate, 99 +/- 12 beats/min). Killing and ingesting the mice required 6-15 min, during which time mean SABP and heart rate were 84 +/- 16 mmHg and 92 +/- 12 beats/min. Pulmonary blood pressure also increased but remained 40-50 mmHg lower than SABP. During stress elicited by tapping the snakes for 5-8 min, heart rate was 94 +/- 6 beats/min but SABP averaged only 44 +/- 11 mmHg. Plasma norepinephrine and epinephrine increased 51- and 26-fold. Plasma glucose increased 58%, hematocrit increased 19%, and plasma volume decreased 19%. It is concluded that blood pressure is markedly affected by behavior and that the sympathetic nervous system appears to play a key role.


Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1803
Author(s):  
Paweł Gać ◽  
Karolina Czerwińska ◽  
Małgorzata Poręba ◽  
Adam Prokopowicz ◽  
Helena Martynowicz ◽  
...  

The aim of the study was to assess the relationship between serum selenium and zinc concentrations (Se-S and Zn-S) and the left ventricle geometry in patients suffering from arterial hypertension. A total of 78 people with arterial hypertension (mean age: 53.72 ± 12.74 years) participated in the study. Se-S and Zn-S were determined in all patients. The type of left ventricular remodelling and hypertrophy was determined by the left ventricular mass index (LVMI) and relative wall thickness (RWT) measured by echocardiography. Se-S and Zn-S in the whole group were 89.84 ± 18.75 µg/L and 0.86 ± 0.13 mg/L. Normal left ventricular geometry was found in 28.2% of patients; left ventricular hypertrophy (LVH) in 71.8%, including concentric remodelling in 28.2%, concentric hypertrophy in 29.5%, and eccentric hypertrophy in 14.1%. LVH was statistically significantly more frequent in patients with Se-S < median compared to patients with Se-S ≥ median (87.2% vs. 56.4%, p < 0.05), as well as in patients with Zn-S < median compared to patients with Zn-S ≥ median (83.8% vs. 60.9%, p < 0.05). In hypertensive patients, older age, higher LDL cholesterol, higher fasting glucose, lower Se-S, and lower Zn-S were independently associated with LVH. In conclusion, in hypertensive patients, left ventricular hypertrophy may be associated with low levels of selenium and zinc in the serum.


2010 ◽  
Vol 16 (3) ◽  
pp. 256-260 ◽  
Author(s):  
M. E. Statsenko ◽  
M. V. Derevjanchenko

Objective. To study the blood pressure variability, morphofunctional parameters of the heart, kidney and metabolic status in hypertensive patients with secondary chronic pyelonephritis. Design and methods. The study included 110 patients: 55 patients with arterial hypertension and secondary chronic pyelonephritis, who underwent surgery for upper urinary tract, and 55 patients with essential arterial hypertension. All patients underwent 24-hour blood pressure monitoring, echocardiography; relative urine density in the morning urine portion, microalbuminuria, blood creatinine were assessed, glomerular fi ltration rate was calculated using MDRD formula. Results. Patients with arterial hypertension and chronic pyelonephritis have signifi cant changes of the blood pressure profi le, and hypertrophy and diastolic left ventricle dysfunction are more frequently observed in this group. A close relation between renal function and the state of the cardiovascular system is established. We also found higher numbers of total cholesterol, the most atherogenic fractions of cholesterol and triglycerides in this group compared to patients with essential hypertension.


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