Peripheral vascular resistance and regional blood flows in hypertensive Dahl rats

1991 ◽  
Vol 261 (4) ◽  
pp. R934-R938 ◽  
Author(s):  
M. A. Boegehold ◽  
L. J. Huffman ◽  
G. A. Hedge
Keyword(s):  
Cardiac Output ◽  
Vascular Resistance ◽  
Salt Intake ◽  
Peripheral Resistance ◽  
Resistance Index ◽  
High Salt ◽  
Renal Vasculature ◽  
Blood Flows ◽  
High Salt Intake ◽  
Regional Blood Flows

The aim of this study was to determine whether different organs undergo similar increases in vascular resistance with hypertension in the Dahl salt-sensitive rat. Cardiac output and organ blood flows were measured with microspheres in anesthetized salt-sensitive and salt-resistant rats fed a high- (7%) or normal- (0.45%) salt diet for 4 wk. High salt intake produced hypertension only in salt-sensitive rats. Cardiac index for the hypertensive group was not different from that for any other group, whereas peripheral resistance index was elevated in proportion to arterial pressure. There were no differences among groups in the fraction of cardiac output supplying the myocardium, intestine, diaphragm, spinotrapezius muscle, or gracilis muscle. The fraction of cardiac output supplying the kidneys was lower in salt-sensitive rats (13%) than in salt-resistant rats (17%) and, among salt-sensitive rats, lowest in the high-salt group. Therefore all the organs studied contribute to increased total peripheral resistance in the hypertensive Dahl rat, with the renal vasculature undergoing the largest resistance increase. Different muscles undergo similar increases in vascular resistance, despite differences in the microvascular abnormalities accompanying salt-induced hypertension.

Systemic and regional hemodynamic effects of endogenous vasopressin stimulation in rats

1982 ◽  
Vol 243 (4) ◽  
pp. H560-H565
Author(s):  
F. Charocopos ◽  
P. Hatzinikolaou ◽  
W. G. North ◽  
H. Gavras
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Vascular Resistance ◽  
Peripheral Resistance ◽  
Base Line ◽  
Blood Flows ◽  
Fluid Load ◽  
Regional Blood Flows ◽  
Blood Pressures ◽  
Specific Antagonist

We investigated the systemic and regional hemodynamic alterations induced in normotensive anephric rats by stimulation of endogenous vasopressin with an acute sodium and fluid load and following vasopressin inhibition with a specific antagonist of its vasoconstricting action. Blood pressure and total peripheral resistance were significantly higher and cardiac output was lower in rats with stimulated vasopressin, and all were reversed to near control levels in rats receiving the vasopressin inhibitor. Regional blood flows were diminished in most organs and local vascular resistance was elevated compared with control animals, but the magnitude of change varied widely. In fact, heart blood flow did not decrease significantly and brain blood flow actually increased indicating small or no change in vascular resistance of these organs. Moreover, fractional distribution of the diminished cardiac output to these organs was significantly higher, so that blood flow to vital organs was maintained at the expense of blood flow to other tissues. In rats that received the vasopressin antagonist after the saline infusion, regional blood flows were similar to those of control animals. Blood pressures at the base line and after hypertonic NaCl infusion correlated closely with the corresponding plasma levels of control and stimulated vasopressin.

Increased organ blood flow in chronic endotoxemia is reversed by nitric oxide synthase inhibition

1994 ◽  
Vol 76 (6) ◽  
pp. 2785-2793 ◽  
Author(s):  
J. Meyer ◽  
F. Hinder ◽  
J. Stothert ◽  
L. D. Traber ◽  
D. N. Herndon ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cardiac Index ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Resistance Index ◽  
No Synthase ◽  
Organ Blood Flow ◽  
Systemic Vascular Resistance Index ◽  
Blood Flows ◽  
Regional Blood Flows

We evaluated regional blood flows in a hyperdynamic sepsis model and the reversal of increased flows by blockade of nitric oxide (NO) synthase. Seven awake sheep were continuously infused with Escherichia coli endotoxin [lipopolysaccharide (LPS), 10 ng.kg-1.min-1] for 48 h. The NO synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME, 25 mg/kg) was injected after 24 h. Blood flows to systemic organs were determined with the radioactive microsphere technique. LPS induced elevation of cardiac index by 36% (P < 0.05) and a fall in systemic vascular resistance index by 37% (P < 0.05) at 0 h [time of L-NAME administration, 24 h after infusion of LPS had begun] L-NAME administration normalized cardiac index [6.1 +/- 0.5 at 4 h posttreatment, 6.1 +/- 0.5 l.min-1.m-2 at -24 h (baseline)] and systemic vascular resistance index (1,333 +/- 105 at 4 h posttreatment, 1,280 +/- 163 dyn.s.cm-5.m2 at -24 h) and reduced all regional blood flows to near-baseline levels for the remainder of the study period (24 h). O2 consumption was unaffected by treatment.

Hemodynamics, fluid volume, and hormonal responses to chronic high-salt intake in dogs

1990 ◽  
Vol 259 (6) ◽  
pp. H1629-H1636 ◽  
Author(s):  
J. E. Krieger ◽  
J. F. Liard ◽  
A. W. Cowley
Keyword(s):  
Angiotensin Ii ◽  
Salt Intake ◽  
Peripheral Resistance ◽  
Plasma Renin ◽  
Total Body Weight ◽  
High Salt ◽  
Plasma Sodium ◽  
Plasma Protein Concentration ◽  
Hormonal Responses ◽  
High Salt Intake

The sequential hemodynamics, fluid and electrolyte balances, and the hormonal responses to a 7-day high-salt (NaCl) intake were investigated in sodium-depleted conscious dogs (n = 6). Studies were carried out in metabolic cages mounted on sensitive load cells, which enabled continuous 24 h/day monitoring of total body weight (TBW) as an index of changes in body water. Beat-by-beat hemodynamics were determined 24 h/day. Water (700 ml/day iv) intake was maintained constant. Daily fluid and electrolyte balances and hormonal analyses were performed. An increase of daily salt intake from 8 to 120 meq increased TBW 251 +/- 44 g (P less than 0.05), which was sustained thereafter. Average 24-h mean arterial pressure (MAP) and heart rate (HR) remained unchanged. Average cardiac output (CO) increased 11% (P less than 0.05) above control values by day 2, while total peripheral resistance (TPR) decreased proportionally. CO and TPR returned to control values only when low salt was resumed. Blood volume (BV) was unchanged on day 2 as indicated by direct measurement of BV (51Cr-labeled red blood cells) or by analysis of plasma protein concentration. A 92-meq (P less than 0.05) sodium retention was observed initially, and plasma sodium concentration increased slightly. Plasma renin activity, angiotensin II, and aldosterone levels decreased significantly, whereas vasopressin and atrial natriuretic peptide levels remained unchanged. In summary, chronic high-salt intake resulted in a net retention of water and sodium with no changes in MAP, HR, or BV. The rise in CO was offset by a reduction in TPR, which appeared at least in part related to angiotensin II suppression.

Prevention of fatal hemorrhagic shock in dog by pretreatment with chronic high-salt diet

1985 ◽  
Vol 249 (3) ◽  
pp. H577-H584
Author(s):  
A. P. Rocchini ◽  
K. P. Gallagher ◽  
M. J. Botham ◽  
J. H. Lemmer ◽  
C. A. Szpunar ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Sodium Chloride ◽  
Hemorrhagic Shock ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Plasma Renin ◽  
High Salt ◽  
High Salt Diet ◽  
Salt Diet ◽  
Blood Flows

The ability of a chronic high-salt diet to prevent fatal hemorrhagic shock was examined in 36 mongrel dogs. Twenty-one dogs received a dietary supplement of 9 g sodium chloride/day for 6 wk, and 15 dogs received the same basic diet for 6 wk but without the sodium chloride supplement. Hemorrhagic shock was induced in all dogs by bleeding into an overhanging sealed reservoir. After 3 h of shock, salt-pretreated dogs had a lower systemic vascular resistance of 0.70 +/- 0.02 versus 1.44 +/- 0.04 mmHg X ml-1 X min X kg (P less than 0.01) and a higher cardiac output of 53 +/- 3 versus 26 +/- 3 ml X min-1 X kg-1 (P less than 0.01) than was observed in controls. At 2.5 h of shock, the salt-pretreated dogs also experienced an increase in gastrointestinal (P less than 0.01), hepatic arterial, (P less than 0.05), kidney (P less than 0.05), brain (P less than 0.01), and heart blood flows (P less than 0.001) compared with 0.5 h of shock, whereas the control dogs experienced no increased flow during this same period. We also observed that after 3 h of hypotension there was a significantly smaller increase in plasma renin activity in the salt-pretreated dogs. Administration of 0.1 U X kg-1 X min-1 of hog renin eliminated the differences in systemic vascular resistance, cardiac output, and survival in five salt-pretreated dogs.

Regional Blood Flows in High-Cardiac-Output Hypertension

1980 ◽  
Vol 59 (s6) ◽  
pp. 355s-356s ◽  
Author(s):  
J. F. Liard
Keyword(s):  
Cardiac Output ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Initial Increase ◽  
Water Load ◽  
Blood Flows ◽  
Vascular Bed ◽  
Regional Blood Flows ◽  
Electromagnetic Flow Meter ◽  
Secondary Rise

1. Mean arterial pressure, cardiac output (electromagnetic flow-meter) and regional blood flows (15 μm radioactive microspheres) were measured repeatedly in eight dogs receiving a salt and water load after renal mass reduction as well as in six control animals. 2. As previously observed, hypertension developed in the salt-loaded dogs with an initial increase in cardiac output followed by a secondary rise in total peripheral resistance. 3. Much of the early increase in cardiac output was distributed to the skeletal muscle vascular bed. 4. Total peripheral resistance changes did not reflect the resistance of individual vascular beds in the early stages of salt and water load hypertension; indeed, resistance in the muscle vascular bed was decreased and that in the splanchnic area and the bone increased on the first day of salt and water load when total peripheral resistance was unchanged.

Regional blood flows in salt loading hypertension in the dog

1981 ◽  
Vol 240 (3) ◽  
pp. H361-H367 ◽  
Author(s):  
J. F. Liard
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Muscle Blood Flow ◽  
Peripheral Resistance ◽  
Salt Loading ◽  
Skeletal Muscle Blood Flow ◽  
Blood Flows ◽  
Regional Blood Flows

An intravenous infusion of isotonic sodium chloride, 196 ml/kg per day, was administered for several days to eight dogs with their renal mass reduced. Mean arterial pressure, cardiac output (electromagnetic flowmeter), and regional blood flows (radioactive microspheres) were measured sequentially and the results compared with those obtained in six control dogs. The salt-loaded animals exhibited on the 1st day of the infusion a 25% increase of arterial pressure and cardiac output. Blood flows to the kidney, the splanchnic area, the skin, and the bone were not significantly changed, whereas skeletal muscle blood flow almost doubled. After several days, cardiac output returned toward control values but pressure remained elevated. Skeletal muscle blood flow, as most other regional flows, did not differ significantly from control values at that time. In four dogs studied 6 h after starting a faster saline infusion, most of the increase in cardiac output was also distributed to the skeletal muscle. Total peripheral resistance changes did not reflect the resistance of individual beds, because vasoconstriction appeared early in some areas but was masked by prominent, although transient, vasodilation in skeletal muscle.

Salt loading augments vascular responses to indomethacin in stroke-prone SHR

1982 ◽  
Vol 243 (3) ◽  
pp. H360-H364
Author(s):  
T. Imaizumi ◽  
A. Takeshita ◽  
T. Ashihara ◽  
M. Nakamura
Keyword(s):  
Vascular Resistance ◽  
Prostaglandin E1 ◽  
Salt Intake ◽  
High Salt ◽  
Salt Loading ◽  
Salt Diet ◽  
Spontaneously Hypertensive ◽  
High Salt Intake ◽  
Endogenous Prostaglandins ◽  
Wistar Kyoto

We examined whether endogenous prostaglandins (PGs) participated in control of hindquarters vascular resistance during salt loading in stroke-prone spontaneously hypertensive rates (SHR-SP). SHR-SP and Wistar-Kyoto rats (WKY) were fed either a normal (0.3% NaCl) or high (8% NaCl) salt diet for 5 wk. High salt increased blood pressure and hindquarter vascular resistance (VR) in SHR-SP (P less than 0.01) but not in WKY. Indomethacin given intravenously increased hindquarter VR in SHR-SP during high salt as well as during normal salt (P less than 0.01) but not in either group of WKY. In SHR-SP the increase in hindquarter VR by PG synthesis inhibitors were two times greater during high salt than during normal salt (P less than 0.01). In addition, hindquarter vasodilatation by bradykinin was greater (P less than 0.05) in SHR-SP during high salt than that during normal salt, but vasodilatation by prostaglandin E1 or nitroglycerin was not different between the two groups. These results suggest that vascular synthesis of endogenous PGs was greater in SHR-SP during high salt than that during normal salt. Increased endogenous PGs may play an important role in the regulation of hindquarter VR during high salt intake in SHR-SP.

Atrial extract: hemodynamics in Wistar-Kyoto and spontaneously hypertensive rats

1985 ◽  
Vol 249 (2) ◽  
pp. H265-H271 ◽  
Author(s):  
B. L. Pegram ◽  
M. B. Kardon ◽  
N. C. Trippodo ◽  
F. E. Cole ◽  
A. A. MacPhee
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Vascular Resistance ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Resistance Index ◽  
Organ Blood Flow ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Atrial Natriuretic

Partially purified low (LMW) and high-(HMW) molecular-weight atrial natriuretic extracts were administered intravenously (540 micrograms protein/kg) to conscious Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats. Both LMW and HMW atrial natriuretic extracts produced an immediate decrease in mean arterial pressure that reached maximum within 5 min and returned to control levels within 30 min. In both strains, cardiac output decreased approximately 14% following administration of LMW. Total peripheral resistance increased only in SHR. Organ blood flow was significantly decreased to skin, brain, heart, kidneys, and splanchnic organs of WKY and to skin, muscle, heart, and splanchnic organs of SHR following administration of LMW. Corresponding increases in organ vascular resistance index were observed in brain, heart, and splanchnic organs of WKY and in skin, heart, and splanchnic organs of SHR. To some extent, the changes in organ blood flow may be a reflection of the decrease in cardiac output induced by LMW. After administration of HMW, no significant changes were observed in cardiac output or total peripheral resistance, although they tended to decrease. Organ vascular resistance was decreased to skin, muscle, brain, and splanchnic organs of SHR. Little difference was observed between WKY and SHR responses to atrial natriuretic extracts. These data indicate that atrial natriuretic extracts have an effect on systemic and regional hemodynamics in conscious rats that differs markedly from those of vasodilators such as nitroglycerin or hydralazine.

Differential Role of Renal Alpha 1 Adreno Receptors Subtypes in Renal Vasculature in Normotensive and Hypertensive Conditions Subjected to High Dietary Salt Load

2021 ◽  
Vol 14 (1) ◽  
pp. 343-349
Author(s):  
Raisa N Kazi
Keyword(s):  
Blood Pressure ◽  
Vascular Resistance ◽  
Vascular Function ◽  
High Salt ◽  
Vascular Pathology ◽  
Adrenergic System ◽  
Renal Vasculature ◽  
High Salt Intake ◽  
Vascular Beds ◽  
Renal Vascular

Chronic high salt intake is well known to be linked to cause an increase in the blood pressure and one of the pathogenic effects of high salt on blood pressure is vascular functional impairment. The effect of sodium on vasculature involves an increase in the vascular resistance that could triggers a rise in the blood pressure. Sodium-induced increase in vascular resistance is primarily independent of any change in blood pressure; however, it could be an initiating factor for increase in the blood pressure. Salt induced increase in the vascular resistance involves alterations in several vasoregulatory mechanisms as evidenced in various vascular beds. A mechanism exhibiting a substantial effect on vascular function is the alpha (α1)-adrenergic system that significantly influences vascular resistance, thereby affecting peripheral vascular resistance and blood pressure. This review focused on the effects of increase dietary sodium intake on the α1-adrenergic system in renal vascular beds under normotensive and hypertensive conditions. Because the α1-adrenergic regulations of renal vascular function and renal hemodynamics affect blood pressure to a great extent, renal vascular assessment was performed. Study reports enhanced renal vascular sensitivity to α1-adrenergic agonist in high sodium normotensive and hypertensive condition, this could be due to functional alterations in the renal α1-adrenoreceptor density. This provide additional evidence on the underlying vascular pathology in salt-induced hypertension.

Effects of haemorrhage and volume expansion on portal–systemic collateral vascular resistance in conscious portal hypertensive rats

1990 ◽  
Vol 78 (2) ◽  
pp. 193-197 ◽  
Author(s):  
Abraham Koshy ◽  
Tatsuya Sekiyama ◽  
Jean-Michel Cereda ◽  
Antoine Hadengue ◽  
Catherine Girod ◽  
...  
Keyword(s):  
Blood Flow ◽  
Body Weight ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Blood Volume ◽  
Vascular Resistance ◽  
Volume Expansion ◽  
Portal Pressure ◽  
Blood Flows ◽  
Regional Blood Flows

1. In order to study the acute effects of blood volume changes on the vascular resistance of portal-systemic collaterals (collateral vascular resistance), a model of total portal vein occlusion with 100% portal-systemic shunts was developed in the rat. In this model, we determined the haemodynamic effects of haemorrhage (1.8 ml/100 g body weight) or intravenous infusion of a volume expander (1.8 ml/100 g body weight). Cardiac output and regional blood flows were measured by the radioactive microsphere method. 2. Haemorrhage significantly reduced arterial pressure from 108 ± 4 to 92 ± 4 mmHg (mean ± sem), cardiac output from 56 ± 4 to 24 ± 2 ml min−1 100 g−1 body weight, portal pressure from 15.1 ± 1.5 to 10.0 ± 1.4 mmHg and portal tributary blood flow from 19.9 ± 2.3 to 8.3 ± 1.4 ml/min. Consequently, collateral vascular resistance significantly increased from 6.6 ± 0.9 × 103 to 11.1 ± 2.0 × 103 kPal−1 s. 3. Volume expansion reduced arterial pressure from 98 ± 3 to 90 ± 3 mmHg, and significantly increased cardiac output from 43 ± 3 to 55 ± 3 ml min−1 100 g−1 body weight, portal pressure from 13.9 ± 0.7 to 16.5 ± 0.8 mmHg and portal tributary blood flow from 16.4 ± 1.3 to 28.2 ± 3.2 ml/min. Consequently, collateral vascular resistance significantly decreased from 7.0 ± 0. 5 × 103 to 4.9 ± 0.4 × 103 kPa l−1 s. 4. This study shows that in rats with portal hypertension, portal-systemic collateral vascular resistance is modified by alterations in blood volume.

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