Inhibition of Adrenaline-Forming Enzyme in the Brain Prevents One-Kidney, One-Clip Hypertension and Deoxycorticosterone Acetate-Salt Hypertension in the Rabbit

1982 ◽  
Vol 63 (6) ◽  
pp. 573-576 ◽  
Author(s):  
C. Rosendorff ◽  
J. R. Melamed ◽  
M. L. Hurwitz ◽  
A. Coull ◽  
A. Jarvis
Keyword(s):  
Blood Pressure ◽  
Blood Pressure Response ◽  
Renal Hypertension ◽  
Pressure Rise ◽  
Deoxycorticosterone Acetate ◽  
Spontaneously Hypertensive ◽  
Arterial Blood ◽  
Salt Hypertension ◽  
The Mean ◽  
The Brain

1. Phenylethanolamine N-methyltransferase (PNMT) converts noradrenaline into adrenaline and brain PNMT is elevated in spontaneously hypertensive and deoxycorticosterone acetate (DOCA)-salt hypertensive rats. In view of the evidence for the involvement of central adrenergic neurons in renal hypertension, we measured the blood pressure response in one-clip, one-kidney Goldblatt hypertensive and DOCA-salt hypertensive rabbits to the PNMT inhibitor SK&F 64139, injected into the lateral cerebral ventricles. 2. Intracerebroventricular injection of SK&F 64139 (10 μg/kg) significantly attenuated the mean arterial blood pressure rise in one-clip, one-kidney and DOCA-salt rabbits, at 4 and 8 weeks. 3. These findings support the idea that hypertension in this animal model requires an intact adrenaline biosynthetic process, and that central catecholaminergic neurons may be involved in the pathogenesis of low-renin volume dependent forms of hypertension.

Vasodilation of cat cerebral arterioles by prostaglandins D2, E2, G2, and I2

1979 ◽  
Vol 237 (3) ◽  
pp. H381-H385 ◽  
Author(s):  
E. F. Ellis ◽  
E. P. Wei ◽  
H. A. Kontos
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Arterial Blood Pressure ◽  
Standard Error ◽  
Arterial Blood ◽  
Cerebral Arterioles ◽  
The Mean ◽  
Dose Dependent ◽  
The Brain

To determine the possible role that endogenously produced prostaglandins may play in the regulation of cerebral blood flow, the responses of cerebral precapillary vessels to prostaglandins (PG) D2, E2, G2, and I2 (8.1 X 10(-8) to 2.7 X 10(-5) M) were studied in cats equipped with cranial windows for direct observation of the microvasculature. Local application of PGs induced a dose-dependent dilation of large (greater than or equal to 100 microns) and small (less than 100 microns) arterioles with no effect on arterial blood pressure. The relative vasodilator potency was PGG2 greater than PGE2 greater than PGI2 greater than PGD2. With all PGs, except D2, the percent dilation of small arterioles was greater than the dilation of large arterioles. After application of prostaglandins in a concentration of 2.7 X 10(-5) M, the mean +/- standard error of the percent dilation of large and small arterioles was, respectively, 47.6 +/- 2.7 and 65.3 +/- 6.1 for G2, 34.1 +/- 2.0, and 53.6 +/- 5.5 for E2, 25.4 +/- 1.8, and 40.2 +/- 4.6 for I2, and 20.3 +/- 2.5 and 11.0 +/- 2.2 for D2. Because brain arterioles are strongly responsive to prostaglandins and the brain can synthesize prostaglandins from its large endogenous pool of prostaglandin precursor, prostaglandins may be important mediators of changes in cerebral blood flow under normal and abnormal conditions.

scholarly journals β-Arrestin–Biased Agonist Targeting the Brain AT 1 R (Angiotensin II Type 1 Receptor) Increases Aversion to Saline and Lowers Blood Pressure in Deoxycorticosterone Acetate–Salt Hypertension

Hypertension ◽  
2020 ◽  
Author(s):  
Mario Zanaty ◽  
Fernando A.C. Seara ◽  
Pablo Nakagawa ◽  
Guorui Deng ◽  
Natalia M. Mathieu ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Central Administration ◽  
Deoxycorticosterone Acetate ◽  
Intracerebroventricular Infusion ◽  
Salt Hypertension ◽  
Saline Solutions ◽  
The Brain ◽  
Biased Agonist

Activation of central AT 1 Rs (angiotensin type 1 receptors) is required for the increased blood pressure, polydipsia, and salt intake in deoxycorticosterone acetate (DOCA)–salt hypertension. TRV120027 (TRV027) is an AT 1 R-biased agonist that selectively acts through β-arrestin. We hypothesized that intracerebroventricular administration of TRV027 would ameliorate the effects of DOCA-salt. In a neuronal cell line, TRV027 induced AT 1a R internalization through dynamin and clathrin-mediated endocytosis. We next evaluated the effect of chronic intracerebroventricular infusion of TRV027 on fluid intake. We measured the relative intake of water versus various saline solutions using a 2-bottle choice paradigm in mice subjected to DOCA with a concomitant intracerebroventricular infusion of either vehicle, TRV027, or losartan. Sham mice received intracerebroventricular vehicle without DOCA. TRV027 potentiated DOCA-induced water intake in the presence or absence of saline. TRV027 and losartan both increased the aversion for saline—an effect particularly pronounced for highly aversive saline solutions. Intracerebroventricular Ang (angiotensin) II, but not TRV027, increased water and saline intake in the absence of DOCA. In a separate cohort, blood pressure responses to acute intracerebroventricular injection of vehicle, TRV, or losartan were measured by radiotelemetry in mice with established DOCA-salt hypertension. Central administration of intracerebroventricular TRV027 or losartan each caused a significant and similar reduction of blood pressure and heart rate. We conclude that administration of TRV027 a selective β-arrestin biased agonist directly into the brain increases aversion to saline and lowers blood pressure in a model of salt-sensitive hypertension. These data suggest that selective activation of AT 1 R β-arrestin pathways may be exploitable therapeutically.

Effects of central and peripheral angiotensin blockade in hypertensive rats

1978 ◽  
Vol 234 (5) ◽  
pp. H629-H637 ◽  
Author(s):  
J. F. Mann ◽  
M. I. Phillips ◽  
R. Dietz ◽  
H. Haebara ◽  
D. Ganten
Keyword(s):  
Blood Pressure ◽  
Renal Hypertension ◽  
Pressure Regulation ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Blood Pressure Decrease ◽  
Different Types ◽  
Angiotensin Blockade ◽  
The Brain ◽  
Goldblatt Hypertension

The angiotensin II (AII) antagonist [Sar1-Ala8]AII (Saralasin) was injected into the brain ventricles (IVT) and intravenously (IV) in five different types of hypertensive unanesthetized rats. Renal hypertension was studied 16-22 days after kidney clipping. Intravenous infusions of cumulative doses (0.1-100 microgram/kg per min) and IVT injections (5-40 microgram) of Saralasin did not change mean arterial pressure (MAP) in controls and in one-clip, one-kidney Goldblatt hypertension, whereas MAP decreased in one-clip, two-kidney Goldblatt hypertension following IV and IVT Saralasin. In two-clip, two kidney hypertensive rats, IVT Saralasin decreased MAP but was ineffective when infused IV. Both IV and IVT Saralasin increased MAP in DOC hypertension. In spontaneously hypertensive (SH) rats, IV Saralasin increased MAP; IVT injection decreased MAP. The effect of IVT Saralasin in SH rats persisted 15-20 h after nephrectomy. We conclude that plasma AII may contribute to peripheral and central mechanisms of blood pressure regulation. The dissociation of the effects of IV and IVT Saralasin and the persistance of blood pressure decrease in nephrectomized SH rats following IVT Saralasin further support a role for locally formed brain angiotensin.

Blood Pressure Response to Central and Peripheral Injection of Angiotensin II and 8-C-Phenylglycine Analogue of Angiotensin II in Rats with Experimental Hypertension

1976 ◽  
Vol 51 (s3) ◽  
pp. 403s-406s
Author(s):  
B. A. Schoelkens ◽  
W. Jung ◽  
R. Steinbach
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Blood Pressure Response ◽  
Renal Hypertension ◽  
Plasma Renin ◽  
Spontaneous Hypertension ◽  
Experimental Hypertension ◽  
Central Administration ◽  
Spontaneously Hypertensive ◽  
Old Rats

1. We have compared the effect of central and peripheral administration of angiotensin II and (1-succinamoyl-5-valine-8-phenylglycine)angiotensin II on blood pressure of male conscious unrestrained rats with normal blood pressure, and with spontaneous hypertension or chronic renal hypertension. 2. After central and peripheral injection of angiotensin II all rats exhibited a significant dose-related increase in blood pressure. 3. Administration of the analogue was without effect in normotensive rats. Ten-weeks-old rats with spontaneous hypertension showed a significant blood pressure decrease after central injection, but an increase after peripheral injection. This centrally induced decrease could not be observed in spontaneously hypertensive rats 14 weeks old. In these animals the analogue increased the blood pressure. In rats with chronic renal hypertension in contrast to peripheral injection, central administration decreased the pressure significantly. 4. Plasma renin activity was not changed after central injection of the analogue in normotensive rats. 5. These observations suggest the participation of the intrinsic brain isorenin-angiotensin system in central blood pressure regulation in these forms of experimental hypertension.

Differential acquisition of specific components of a classically conditioned arterial blood pressure response in rat

2005 ◽  
Vol 289 (3) ◽  
pp. R784-R788 ◽  
Author(s):  
Yasser M. El-Wazir ◽  
Sheng-Gang Li ◽  
Daniel T. Williams ◽  
Aletia G. Sprinkle ◽  
David R. Brown ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Response Pattern ◽  
Blood Pressure Response ◽  
Pressor Response ◽  
Orienting Response ◽  
Arterial Blood ◽  
Differential Acquisition ◽  
Traditional Paradigm ◽  
Classically Conditioned ◽  
The Brain

Presenting a 15-s pulsed tone, the conditional stimulus (CS+), followed by 0.5-s tail shock, to a well-trained rat causes a sudden, but transient, pressor response (C1). Blood pressure (BP) then drops before increasing again (C2). A steady tone of the same frequency never followed by a shock (a discriminative stimulus, or CS−) evokes a C1 but not a C2 response. Experiment 1 tested the hypothesis that this BP response pattern does not depend on the nature of the tone (i.e., pulsed vs. steady) used for CS+ and CS−. The tones were reversed from the traditional paradigm, above, in nine rats. The C1 BP increase for a steady-tone CS+ (+4.8 ± 1.9 mmHg, mean change ± SE) and a pulsed CS− (+2.9 ± 1.3 mmHg) did not differ. Conversely, C2 showed a clear discrimination (CS+: +5.1 ± 1.2 mmHg, CS−: +0 .7 ± 0.8 mmHg; P < 0.05). Experiment 2 tested the hypothesis that the C1 and C2 BP responses first appear at different times during training. On training day 1, five 15-s pulsed tones (CS+) were presented to each of 18 rats; the last tone was followed by a tail shock. Likewise, five steady CS− tones never followed by shock were given. Training continued for 2 more days, with each CS+ followed by shock. At the end of day 2, CS+ evoked a C1 BP response (+3.9 ± 0.9 mmHg) but no C2 (+0.6 ± 0.4 mmHg, not significant vs. pretone). By the end of day 3, CS+ evoked a significant (vs. baseline) C1 (+7.3 ± 1.4 mmHg) and C2 (+3.3 ± 0.8 mmHg). Conversely, although CS− evoked a C1 response (3.5 ± 1.3 mmHg), there was no C2 (+0.7 ± 0.5 mmHg; not significant). We conclude that 1) C1 and C2 are acquired at different rates, 2) early in training C1 is an orienting response evoked by both tones, and 3) C2 is only acquired as an animal learns to associate the CS+ tone with shock. This suggests that C1 and C2 are controlled by different processes in the brain.

scholarly journals PRODUCTION OF ANTIRENIN TO HOMOLOGOUS RENIN AND ITS EFFECT ON EXPERIMENTAL RENAL HYPERTENSION

1964 ◽  
Vol 119 (3) ◽  
pp. 425-432 ◽  
Author(s):  
Sharad D. Deodhar ◽  
Erwin Haas ◽  
Harry Goldblatt
Keyword(s):  
Blood Pressure ◽  
Large Scale ◽  
Renal Hypertension ◽  
Chronic Phase ◽  
Partial Purification ◽  
Subcutaneous Injections ◽  
Progressive Development ◽  
Arterial Blood ◽  
Experimental Renal Hypertension ◽  
The Mean

1. Procedures are described for the extraction and partial purification of dog renin, on a large scale, as well as for the acetylation of rat, rabbit, and dog renin. 2. Untreated homologous renin was not antigenic in rat, rabbit, or dog, but the acetylation of homologous renin made it antigenic. 3. Immunization of rats, rabbits, and dogs, with acetylated rat, rabbit, and dog renin, respectively, resulted in each case in the development of anti-renin to the homologous, untreated, as well as to the acetylated renin. 4. The progressive development of antirenin as a result of repeated, subcutaneous injections of acetylated dog renin, in a dog with experimental renal hypertension for more than 6 years, was accompanied by a correspondingly progressive fall of the mean arterial blood pressure to the prehypertensive level. This points up the important part played by the renin-angiotensin mechanism in the maintenance of the hypertension, even in the chronic phase of experimental renal hypertension.

Impairment of Cerebral Autoregulation during the Development of Chronic Cerebral Vasospasm after Subarachnoid Hemorrhage in Primates

Neurosurgery ◽  
1991 ◽  
Vol 28 (1) ◽  
pp. 41-48 ◽  
Author(s):  
Hiroaki Takeuchi ◽  
Yuji Handa ◽  
Hidenori Kobayashi ◽  
Ilirokazu Kawano ◽  
Minoru Hayashi
Keyword(s):  
Blood Pressure ◽  
Subarachnoid Hemorrhage ◽  
Arterial Blood Pressure ◽  
Cerebral Vasospasm ◽  
Conduction Time ◽  
Arterial Blood ◽  
The Mean ◽  
The Right ◽  
Chronic Cerebral Vasospasm ◽  
The Brain

Abstract We studied the impairment of autoregulation of cerebral blood flow (CBF) and its effect on the electrical activity of the brain during the development of chronic cerebral vasospasm after subarachnoid hemorrhage, using a vasospasm model in primates. Fourteen animals were divided into two groups: a clot group (8) and a sham-operated group (6). To induce subarachnoid hemorrhage, all the animals underwent craniectomy, and in the clot group, the autologous blood clot was located around the arteries dissected free from the arachnoid membrane. Cerebral angiography was performed before subarachnoid hemorrhage and 7 days after (Day 7). On Day 7, regional CBF in the parietal lobe—measured by the hydrogen clearance method—and central conduction time were studied during either graded hypertension or hypotension. In the clot group, the mean vessel caliber of the cerebral arteries on the right side (clot side) of the circle of Willis showed significant (P&lt;0.01) reduction (more than 40%) as compared with the values on the contralateral, non-clot side. The values for the bilateral parietal CBF in the sham-operated group and the left parietal CBF in the clot group were fairly constant when the mean arterial blood pressure (MABP) was in the range of 60 to 160 mm Hg. In the clot group, right parietal CBF was significantly (P &lt; 0.05) smaller than that on the left side at an MABP level of 40 to 100 mm Hg, and increased at an MABP level of 180 mm Hg. The right parietal CBF increased as the arterial blood pressure increased, showing impairment of autoregulation. The central conduction time on the right side in the clot group was significantly (P&lt;0.05) prolonged at an MABP of 40 mm Hg. It is suggested that impairment of autoregulation is strongly affected by the development of cerebral vasospasm and that, in this state, a decrease in cerebral perfusion pressure easily depresses the electrical function of the brain.

scholarly journals On the Pathology of the dropsy produced by obstruction of the superior and inferior venœ and the portal vein.— Preliminary communication

1907 ◽  
Vol 79 (532) ◽  
pp. 267-283 ◽  
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Portal Vein ◽  
Mean Arterial Blood Pressure ◽  
Normal Limit ◽  
The Body ◽  
Diastolic Filling ◽  
Arterial Blood ◽  
Preliminary Communication ◽  
The Mean

In August, 1903, I published a paper in the ‘Journal of Pathology’(1) in which I demonstrated a method experimentally producing uncompensated hear disease in an animal, which was compatible with life. This method consisted in diminishing the size of the pericardial sac by stitches, so that the diastolic filling of the heart was impeded. The main symptoms of this condition were dropsy and diminution in the amount of urine excreted. As the immediate result of this interference with the action of the heart, there occurred a rise of pressure throughout the whole systemic venous system extending as far back as the capillaries, and a fall of the mean arterial blood-pressure. Further, I found that the pressure in all the veins fell to the normal limit again within the space of about one hour, and that subsequently when dropsy was being produced, the vanous pressure in all parts of the body was normal, and the arterial pressure had almost recovered itself.

scholarly journals An Estimation Method of Continuous Non-Invasive Arterial Blood Pressure Waveform Using Photoplethysmography: A U-Net Architecture-Based Approach

Sensors ◽  
2021 ◽  
Vol 21 (5) ◽  
pp. 1867
Author(s):  
Tasbiraha Athaya ◽  
Sunwoong Choi
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Health ◽  
Estimation Method ◽  
Absolute Error ◽  
British Hypertension Society ◽  
Non Invasive ◽  
Arterial Blood ◽  
Blood Pressure Waveform ◽  
The Mean ◽  
Mimic Iii

Blood pressure (BP) monitoring has significant importance in the treatment of hypertension and different cardiovascular health diseases. As photoplethysmogram (PPG) signals can be recorded non-invasively, research has been highly conducted to measure BP using PPG recently. In this paper, we propose a U-net deep learning architecture that uses fingertip PPG signal as input to estimate arterial BP (ABP) waveform non-invasively. From this waveform, we have also measured systolic BP (SBP), diastolic BP (DBP), and mean arterial pressure (MAP). The proposed method was evaluated on a subset of 100 subjects from two publicly available databases: MIMIC and MIMIC-III. The predicted ABP waveforms correlated highly with the reference waveforms and we have obtained an average Pearson’s correlation coefficient of 0.993. The mean absolute error is 3.68 ± 4.42 mmHg for SBP, 1.97 ± 2.92 mmHg for DBP, and 2.17 ± 3.06 mmHg for MAP which satisfy the requirements of the Association for the Advancement of Medical Instrumentation (AAMI) standard and obtain grade A according to the British Hypertension Society (BHS) standard. The results show that the proposed method is an efficient process to estimate ABP waveform directly using fingertip PPG.

Sign in / Sign up

Export Citation Format

Share Document