Chronic effects of a physiological dose of ANP on arterial pressure and renin release

1990 ◽  
Vol 258 (5) ◽  
pp. H1491-H1497
Author(s):  
S. D. Kivlighn ◽  
T. E. Lohmeier ◽  
H. M. Yang ◽  
Y. Shin
Keyword(s):  
Arterial Pressure ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Renal Perfusion ◽  
Renin Release ◽  
Long Term Effects ◽  
Chronic Effects ◽  
Physiological Dose

To determine the long-term effects of a physiological dose of atrial natriuretic peptide (ANP) on renin release, the renin response to reductions in renal arterial pressure (RAP) was studied during 1) control conditions and 2) acute and 3) chronic (5 days) intravenous infusion (5 ng.kg-1.min-1) of alpha-human ANP in conscious dogs maintained on a normal sodium intake. Renal perfusion pressure was servo controlled at reduced levels with an inflatable occluder placed around the abdominal aorta just above the renal arteries. Under control conditions, reducing RAP by 30 and 40 mmHg increased plasma renin activity (PRA) 4- to 5- and 9- to 10-fold, respectively. Acute ANP infusion had no significant effect on either basal levels of PRA or the PRA response to reduced RAP. During chronic ANP infusion there was a two- to threefold increment in plasma ANP concentration and approximately a twofold increase in urinary sodium excretion on day 1; however, there were no significant long-term changes in mean arterial pressure, basal PRA, or the levels of PRA achieved during reductions in RAP. These findings indicate that the changes in plasma ANP concentration that occur under normal physiological conditions do not appreciably alter either basal PRA or renin release in response to renal hypotension in conscious sodium-replete dogs studied under resting conditions.

Role of nitric oxide in the arterial pressure and renal adaptations to long-term changes in sodium intake

1997 ◽  
Vol 272 (4) ◽  
pp. R1162-R1169 ◽  
Author(s):  
R. D. Manning ◽  
L. Hu ◽  
J. F. Reckelhoff
Keyword(s):  
Nitric Oxide ◽  
Arterial Pressure ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Control Group ◽  
High Sodium ◽  
Sodium Sensitivity ◽  
High Sodium Intake

The goals of this study were to determine whether long-term nitric oxide (NO) synthesis inhibition in dogs results in an increase in the sodium sensitivity of arterial pressure and whether changes in plasma renin activity or the plasma concentrations of arginine vasopressin (AVP) and aldosterone play an important role in this hypertension. Studies were conducted in a control group and groups that received NO inhibition with N(G)-nitro-L-arginine methyl ester (L-NAME) at 10 or 25 microg x kg(-1) x min(-1). Each group was challenged with normal, low, and high sodium intake for periods of 5 days each. Urinary nitrate + nitrite excretion (UNOx) more than doubled in the control group during high sodium intake. In both L-NAME groups, UNOx decreased significantly, there was a hypertensive shift in the relation between urinary sodium excretion and arterial pressure, and urinary sodium excretion remained normal even in the high-sodium intake period. L-NAME infusion did not change the sodium sensitivity of arterial pressure or plasma renin activity, plasma aldosterone, and plasma AVP. In conclusion, the data suggest that, in dogs, increases in NO synthesis are not necessary to excrete a chronic sodium load, and decreases in NO do not increase the sodium sensitivity of arterial pressure.

Acute and chronic actions of bradykinin on renal function and arterial pressure

1985 ◽  
Vol 248 (1) ◽  
pp. F87-F92 ◽  
Author(s):  
J. P. Granger ◽  
J. E. Hall
Keyword(s):  
Arterial Pressure ◽  
Renal Plasma Flow ◽  
Urine Volume ◽  
Plasma Renin ◽  
Urinary Sodium Excretion ◽  
Renal Perfusion ◽  
Acute Effects ◽  
Plasma Aldosterone Concentration ◽  
Control Value ◽  
Renal Vascular

The present study was designed to examine the acute and chronic effects of increased levels of circulating bradykinin (BK) on control of renal hemodynamics, electrolyte excretion, and arterial pressure. Intrarenal infusion of BK (50 ng X kg-1 X min-1) for 60 min in five anesthetized dogs with renal perfusion pressure maintained at a constant level of 108 +/- 1 mmHg had no significant effect on glomerular filtration rate (GFR), whereas it increased renal blood flow (RBF) from a control value of 230 +/- 14 to 282 +/- 18, 266 +/- 15, and 253 +/- 17 ml/min after 15, 30, and 60 min of infusion, respectively. Acute intrarenal infusion of BK also increased urine volume (UV) from 0.255 +/- 0.044 to 0.523 +/- 0.103 ml/min and urinary sodium excretion (UNaV) from 5.72 +/- 1.5 to 13.7 +/- 3.4 mueq/min. To determine whether the potent acute effects of BK on RBF, UV, and UNaV lead to a chronic reduction in arterial pressure, BK (50 ng X kg-1 X min-1) was infused intrarenally for 7 days in conscious dogs. Intrarenal infusion of BK for 7 days had no significant effect on GFR, UNaV, UV, or arterial pressure. However, BK elevated renal plasma flow and decreased renal vascular resistance throughout the 7 days of infusion. Chronic intrarenal BK infusion caused no significant changes in plasma renin activity or plasma aldosterone concentration. Results from these studies indicate that although increased levels of bradykinin in the renal circulation can have potent acute effects on RBF, UV, and UNaV, these effects on UV and UNaV are not sustained and therefore do not result in long-term changes in arterial pressure.

Glucocorticoid Inhibition of Mineralocorticoid Action in the Rat

1984 ◽  
Vol 67 (3) ◽  
pp. 329-335 ◽  
Author(s):  
C. J. Kenyon ◽  
N. A. Saccoccio ◽  
D. J. Morris
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Plasma Sodium ◽  
Long Term Effects ◽  
Physiological Dose ◽  
Acute Changes ◽  
Adrenalectomized Rats

1. The mineralocorticoid activity of corticosterone based on acute changes in urinary Na+/K+ ratios in adrenalectomized rats was 1000 times less than that of aldosterone. However, corticosterone had only kaliuretic actions whereas aldosterone had both antinatriuretic and kaliuretic properties. Corticosterone inhibited the antinatriuretic actions of aldosterone. 2. Adrenalectomized rats infused continuously with a physiological dose of corticosterone (1 mg/day) were 5 times less sensitive to the antinatriuretic and 25 times less sensitive to the kaliuretic actions of aldosterone when administered acutely than were control adrenalectomized rats. 3. The long term effects of infusions of physiological doses of aldosterone and corticosterone were assessed in adrenalectomized rats maintained in metabolic cages. Aldosterone lowered plasma renin activity and reduced fluid (0.3% NaCl) intake; these effects were diminished when aldosterone and corticosterone were infused simultaneously. Plasma renin activity and fluid intake were correlated in long term infusion experiments. Both hormones had hypokalaemic effects but these were not additive. Corticosterone, but not aldosterone, increased systolic blood pressure and plasma sodium levels. 4. We conclude that glucocorticoid effects on water and electrolyte metabolism are different from those of mineralocorticoids, that glucocorticoids may antagonize mineralocorticoid effects and that interactions between mineralocorticoids and glucocorticoids may be important in long term blood pressure regulation.

Pressure-dependent renin release: effects of sodium intake and changes of total body sodium

1999 ◽  
Vol 277 (2) ◽  
pp. R548-R555 ◽  
Author(s):  
Erdmann Seeliger ◽  
Katrin Lohmann ◽  
Benno Nafz ◽  
Pontus B. Persson ◽  
H. Wolfgang Reinhardt
Keyword(s):  
Sodium Intake ◽  
Plasma Renin ◽  
Renal Perfusion ◽  
Renin Release ◽  
Response Curves ◽  
Exponential Relationship ◽  
High Sodium ◽  
Body Sodium ◽  
Total Body ◽  
The Impact

The impact of sodium intake and changes in total body sodium (TBS) for the setting of pressure-dependent renin release (PDRR) was studied in freely moving dogs. An aortic cuff allowed servo control of renal perfusion pressure (RPP) at preset values. Protocols were 1) high sodium intake (HSI), 2) low sodium intake (LSI), 3) TBS moderately increased (+3.1 mmol Na/kg body wt) by 20% reduction of RPP for 2–4 days, 4) large increase of TBS (+8.2) by combining protocol 3 with aldosterone infusion, and 5) TBS reduced (−3.1) by peritoneal dialyses. Twenty-four-hour time courses of arterial plasma renin activity (PRA) revealed that LSI increased PRA for the first 10 h only; afterward PRA did not differ between LSI and HSI. Reduced TBS increased PRA constantly, and the large increase of TBS constantly reduced PRA. PDRR stimulus-response curves (assessed 20 h after last sodium intake) revealed an exponential relationship in each protocol. PDRR was not changed by different sodium intake. Conversely, reduced TBS increased PDRR markedly, whereas the large increase of TBS suppressed it. Thus an inverse relationship between TBS and PRA, i.e., a TBS-dependent renin release, was found. This relationship was enhanced by decreasing RPP. This interplay between TBS-dependent renin release and PDRR allows the organism a differentiated reaction to changes in TBS and arterial pressure.

Acute, medium and long-term effects of yellow sand and air pollutants on allergy and biomarker search

Impact ◽  
2020 ◽  
Vol 2020 (3) ◽  
pp. 63-65
Author(s):  
Tomomi Higashi
Keyword(s):  
Air Pollutants ◽  
Genetic Factors ◽  
Long Term Effects ◽  
Emergency Rooms ◽  
Improve Treatment ◽  
Treatment And Prevention ◽  
Chronic Effects ◽  
Difficulty Breathing ◽  
Acute And Chronic Effects

Talk to any allergy sufferer and they will tell you how awful it can be. Runny noses, itchy eyes, coughing and difficulties breathing. For many these symptoms rise only to the level of annoyance and can be avoided by steering clear of the source of their allergy. What many people don't realise though is that allergies can become a far more serious issue for a large segment of the population. Shortness of breath and difficulty breathing due to allergies bring many people to emergency rooms and these are just the acute symptoms. Along with the potential for an allergic attack during a windy or dusty day, researchers and medical professionals are beginning to recognise that there are chronic, long term effects associated with allergies. In order to mitigate both the acute and chronic effects of allergies a better understanding of how genetic factors combine with environmental conditions to produce the ranges of symptoms and effects of allergy suffers is needed. Professor Tomomi Higashi, from the Department of Hygiene at Kanazawa University in Japan, is an expert in this field and is currently working to improve treatment and prevention of allergic disease.

LONG TERM EFFECTS OF THYROID STIMULATING HORMONE AND INSULIN ON INTRACELLULAR pH IN FRTL-5 CELLS

1992 ◽  
Vol 133 (2) ◽  
pp. R9-R11
Author(s):  
A.M. Wood ◽  
S.P. Bidey ◽  
J. Soden ◽  
W.R. Robertson
Keyword(s):  
Intracellular Ph ◽  
Small Groups ◽  
Thyroid Stimulating Hormone ◽  
Ph Sensitive ◽  
Long Term Effects ◽  
Bicarbonate Ions ◽  
Chronic Effects ◽  
Petri Dishes ◽  
Presence And Absence

ABSTRACT We have studied the chronic effects of TSH (100μU/ml) and insulin (10μg/ml) on intracellular pH (pHi) in FRTL-5 cells using the pH sensitive probe 2′7-bis (2-carboxyethyl-5′-6′) carboxyfluorescein. FRTL-5 cells were cultured on Petri dishes either in the presence of 4H, ie. Coons F-12 containing cortisol (10nM), transferrin (0.5μg/ml), glycyl-histidyl lysine acetate (10ng/ml) and somatostatin (10μg/ml), or with 4H+insulin (5H), 4H+TSH, or 4H+TSH+insulin (6H). pHi was measured in small groups of cells by microspectrofluorimetry both in the presence and absence of bicarbonate ions after cells had been deprived of serum for at least a day. In

Effects of hypoproteinemia on renal hemodynamics, arterial pressure, and fluid volume

1987 ◽  
Vol 252 (1) ◽  
pp. F91-F98
Author(s):  
R. D. Manning
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sodium Excretion ◽  
Sodium Intake ◽  
Renal Plasma Flow ◽  
Urinary Sodium Excretion ◽  
Renal Hemodynamics ◽  
Fluid Volume ◽  
Urinary Sodium ◽  
Plasma Aldosterone Concentration

The effects of long-term hypoproteinemia on renal hemodynamics, arterial pressure, and fluid volume were studied in eight conscious dogs over a 34-day period. Plasma protein concentration (PPC) was decreased by daily plasmapheresis, and the effects of decreasing and increasing sodium intake were measured. By the 12th day of plasmapheresis, during which sodium intake was 30 meq/day, PPC had decreased to 2.5 g/dl from a control value of 7.2 g/dl, mean arterial pressure had decreased to 78% of control, glomerular filtration rate (GFR) was 75.2% of control, and urinary sodium excretion was decreased. By day 18 of plasmapheresis, estimated renal plasma flow (ERPF) was decreased to 60% of control due to the decreased arterial pressure and an increase in renal vascular resistance. Also, plasma renin activity and plasma aldosterone concentration were both increased, and the relationship between mean arterial pressure and urinary sodium excretion was distinctly shifted to the left along the arterial pressure axis. In contradistinction to acute experiments, chronic hypoproteinemia results in decreases in GFR, ERPF, and urinary sodium excretion and has marked effects on both fluid volume and arterial pressure regulation.

Effects of meclofenamate on the renin response to aortic constriction in the rat

1984 ◽  
Vol 247 (3) ◽  
pp. R546-R551 ◽  
Author(s):  
D. Villarreal ◽  
J. O. Davis ◽  
R. H. Freeman ◽  
W. D. Sweet ◽  
J. R. Dietz
Keyword(s):  
Perfusion Pressure ◽  
Plasma Renin ◽  
Renal Perfusion ◽  
Renin Release ◽  
Aortic Constriction ◽  
Renal Perfusion Pressure ◽  
Inhibition Of Prostaglandin Synthesis ◽  
Intact Kidney ◽  
Stimulus Secretion Coupling

This study examines the role of the renal prostaglandin system in stimulus-secretion coupling for renal baroreceptor-dependent renin release in the anesthetized rat. Changes in plasma renin activity (PRA) secondary to suprarenal aortic constriction were evaluated in groups of rats with a single denervated nonfiltering kidney (DNFK) with and without pretreatment with meclofenamate. Suprarenal aortic constriction was adjusted to reduce renal perfusion pressure to either 100 or 50 mmHg. In addition, similar experiments were performed in rats with a single intact filtering kidney. Inhibition of prostaglandin synthesis with meclofenamate failed to block or attenuate the increase in PRA in response to the decrement in renal perfusion pressure after both severe and mild aortic constriction for both the DNFK and the intact-kidney groups. The adequacy of prostaglandin inhibition was demonstrated by complete blockade with meclofenamate of the marked hypotensive and hyperreninemic responses to sodium arachidonate. The results in the DNFK indicate that in the rat, renal prostaglandins do not function as obligatory mediators of the isolated renal baroreceptor mechanism for the control of renin release. Also the findings in the intact filtering kidney suggest that prostaglandins are not essential in the renin response of other intrarenal receptor mechanisms that also are stimulated by a reduction in renal perfusion pressure.

scholarly journals Role of the endothelium-dependent relaxing factor nitric oxide on renal function.

1992 ◽  
Vol 2 (9) ◽  
pp. 1371-1387 ◽  
Author(s):  
J C Romero ◽  
V Lahera ◽  
M G Salom ◽  
M L Biondi
Keyword(s):  
Nitric Oxide ◽  
Renal Function ◽  
Perfusion Pressure ◽  
Sodium Intake ◽  
Systemic Circulation ◽  
Renal Perfusion ◽  
Renin Release ◽  
High Sodium ◽  
Renal Perfusion Pressure

The role of nitric oxide in renal function has been assessed with pharmacologic and physiologic interventions. Pharmacologically, the renal vasodilation and, to some extent, the natriuresis produced by endothelium-dependent vasodilators such as acetylcholine and bradykinin are mediated by nitric oxide and also by prostaglandins. However, prostaglandins and nitric oxide do not participate in the renal effects produced by endothelium-independent vasodilators such as atrial natriuretic peptide, prostaglandin I2, and nitroprusside. Physiologically, nitric oxide and prostaglandins exert a strong regulation on the effects produced by changes in renal perfusion pressure. Increments in renal perfusion pressure within the range of RBF autoregulation appear to inhibit prostaglandin synthesis while simultaneously enhancing the formation of nitric oxide. Nitric oxide modulates autoregulatory vasoconstriction and at the same time inhibits renin release. Conversely, a decrease of renal perfusion pressure to the limit of or below RBF autoregulation may inhibit the synthesis of nitric oxide but may trigger the release of prostaglandins, whose vasodilator action ameliorates the fall in RBF and stimulates renin release. Nitric oxide and prostaglandins are also largely responsible for mediating pressure-induced natriuresis. However, unlike prostaglandins, mild impairment of the synthesis of nitric oxide in systemic circulation produces a sustained decrease in sodium excretion, which renders blood pressure susceptible to be increased during high-sodium intake. This effect suggests that a deficiency in the synthesis of nitric oxide could constitute the most effective single disturbance to foster the development of a syndrome similar to that seen in salt-sensitive hypertension.

Steady-state arterial pressure-urinary output relationships during ovine pregnancy

1992 ◽  
Vol 263 (5) ◽  
pp. R1141-R1146
Author(s):  
E. W. Quillen ◽  
B. S. Nuwayhid
Keyword(s):  
Renal Function ◽  
Steady State ◽  
Arterial Pressure ◽  
Sodium Intake ◽  
Control Level ◽  
Urine Volume ◽  
Urinary Sodium Excretion ◽  
Pregnant Sheep ◽  
Plasma Angiotensin ◽  
Steady State Levels

To determine the effects of long-term changes in sodium intake on mean arterial pressure (MAP) regulation during pregnancy, nonpregnant (n = 16) and 110- to 140-day pregnant (n = 13) ewes received total daily sodium intakes of 10, 30, 100, 400, and 1,200 mmol for 7 days. The sheep were housed in metabolism cages and MAP was monitored 24 h/day. Urinary sodium excretion (UNaV) followed changes in sodium intake, with steady-state levels being achieved with similar degrees of rapidity (2-3 days) in nonpregnant and pregnant sheep. At 10 mmol/day sodium intake, MAP was lower (79 +/- 1 vs. 82 +/- 2 mmHg; P < 0.01) and water intake (2,275 +/- 494 vs. 3,286 +/- 725 ml/day; P < 0.001) and 24-h urine volume (1,454 +/- 279 vs. 2,299 +/- 496 ml/day; P < 0.01) were greater in pregnant sheep. All of these variables exhibited direct relationships with increases in sodium intake. Plasma angiotensin II (pANG II) was increased in pregnancy (10.6 +/- 1.6 vs. 24.5 +/- 6.3 pg/ml; P < 0.001) at 10 mmol/day. Elevation of sodium intake suppressed pANG II to minimal levels in nonpregnant sheep, but to only 25% of the control level in pregnant sheep. During pregnancy, the renal function curve representing the steady-state MAP-UNaV relationship was shifted to lower MAP setpoint, but the sodium sensitivity of MAP was unchanged. Also, the inverse relationship of sodium intake and pANG II was blunted, suggesting a reduced role for ANG II in the maintenance of renal function during pregnancy.

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