PubMed Health⌕ Search

Biomedical subjects

W P Anderson

Publications and source records attributed to W P Anderson.

At least 19 recordsLinked to original sources
PubMed1992

Pet ownership and risk factors for cardiovascular disease.

OBJECTIVE: To compare risk factors for cardiovascular disease in pet owners and non-owners. DESIGN AND PATIENTS: Accepted risk factors for cardiovascular disease were measured in 5741 participants attending a free, screening clinic at the Baker Medical Research Institute in Melbourne. Blood pressure, plasma cholesterol and triglyceride values were compared in pet owners (n = 784) and non-owners (n = 4957). RESULTS: Pet owners had significantly lower systolic blood pressure and plasma triglycerides than non-owners. In men, pet owners had significantly lower systolic but not diastolic blood pressure than non-owners, and significantly lower plasma triglyceride levels, and plasma cholesterol levels. In women over 40 years old, systolic but not diastolic pressure was significantly lower in pet owners and plasma triglycerides also tended to be lower. There were no differences in body mass index and self-reported smoking habits were similar, but pet owners reported that they took significantly more exercise than non-owners, and ate more meat and "take-away" foods. The socioeconomic profile of the pet owners and non-owners appeared to be comparable. CONCLUSIONS: Pet owners in our clinic population had lower levels of accepted risk factors for cardiovascular disease, and this was not explicable on the basis of cigarette smoking, diet, body mass index or socioeconomic profile. The possibility that pet ownership reduces cardiovascular risk factors should therefore be investigated.

Animals↗
PubMed1992

Distribution of sympathetic neuroeffector junctions in the juxtaglomerular region of the rabbit kidney.

Two structurally distinct types of sympathetic axon (Type I and Type II) have recently been identified in the renal cortex of the rat and the rabbit. This study describes the distribution and density of the neuroeffector junctions made by these two types of axon on the different tissues from the juxtaglomerular region of the rabbit renal cortex. Immunohistochemical studies showed that tyrosine hydroxylase-positive axons were located only in regions adjacent to the arteries and arterioles in the renal cortex. Ultrastructural studies of the juxtaglomerular region indicated that both types of axon formed junctions on vascular smooth muscle cells, epithelial cells of proximal tubules and renin-secreting granular epithelioid cells. The density of neuromuscular junctions (18 x 10(3)/mm2 of vessel surface) was more than twice as high on the afferent arteriole as on the efferent arteriole or proximal tubules immediately adjacent to the glomerular arterioles (both about 6 x 10(3)/mm2). The junction density on granular epithelioid cells was much lower (about 2 x 10(3)/mm2) and were rarely observed on the distal tubule. Afferent arterioles preferentially received junctions from Type I axons at a relatively high density (14.2 x 10(3)/mm2) whereas junctions formed by Type II axons were less selectively distributed and occurred at lower densities on all other tissues (range, 1-6.3 x 10(3)/mm2). Presynaptic membrane specialisations were identified only at junctions on arterioles and granular epithelioid cells and occurred more frequently at Type I than at Type II junctions. The data suggest that the predominant effect of the sympathetic innervation in the juxtaglomerular region of the renal cortex is on the afferent arteriole and that the two axon types within the kidney may have different functions.

Animals↗
PubMed1992

Morphometric analysis of the actions of angiotensin II on renal arterioles and glomeruli.

To study the effects of angiotensin II on afferent and efferent arteriole diameters and on intraglomerular dimensions, angiotensin II (20 ng.kg-1.min-1) or saline vehicle was infused intravenously for 20 min into anesthetized rabbits pretreated with enalapril. Both kidneys were perfusion fixed (glutaraldehyde), and vascular casts were made of the right kidneys using methacrylate. Morphometric analysis of the left kidneys using transmission electron microscopy revealed no significant effects of angiotensin II within the glomerulus, including the degree of mesangial contraction. The diameters of the afferent and efferent arteriole casts from the right kidneys were measured at 20, 50, and 75 microns from the glomerulus by scanning electron microscopy. In the outer cortex the mean diameters of the afferent and efferent arterioles were 14.1 +/- 0.8 and 9.7 +/- 0.5 microns, respectively, in the angiotensin II-infused rabbits, significantly less than in the control (vehicle) rabbits, 17.0 +/- 0.7 microns (P less than 0.001) and 10.7 +/- 0.4 microns (P less than 0.005), respectively. Calculation of the relative changes in vascular resistance, however, indicated that the effects of angiotensin II on efferent arteriole resistance (average difference 2.4 +/- 1.2 units/microns) were significantly greater per unit length than the effects on afferent arteriole resistance (average difference 0.9 +/- 0.3 units/microns). Thus infused angiotensin II caused greater reduction in afferent arteriolar diameter than in efferent, but the calculated increase in vascular resistance per micron was greater in efferent vessels due to their smaller resting diameter.

Angiotensin II↗
PubMed1991

Glomerular ultrafiltration in rabbits with superficial glomeruli.

The determinants of glomerular ultrafiltration in superficial glomeruli of a strain of English cross-breed rabbits have been studied using micropuncture techniques. Mean arterial blood pressure in the anaesthetised rabbits was 70 +/- 2 mmHg. The glomerular filtration rate in the kidney prepared for micropuncture was 4.4 +/- 0.4 ml/min, the filtration fraction was 22 +/- 1% and renal blood flow was 33 +/- 3 ml/min, and these values were comparable to values in conscious rabbits. Glomerular capillary pressure (Pgc) averaged 31 +/- 1 mmHg, the single-nephron glomerular filtration rate (SNGFR) averaged 25 +/- 2 nl/min, and the mean ultrafiltration pressure (calculated using the whole-kidney filtration fraction) averaged 7 +/- 1 mmHg. A net positive pressure at the efferent end of the glomerular capillaries (4.4 +/- 0.9 mmHg) indicated that a state of filtration pressure disequilibrium existed, under the experimental conditions of this study, in rabbit glomeruli. The calculated glomerular ultrafiltration coefficient (Kf) was 0.08 +/- 0.01 nl s-1 mmHg-1. Thus, compared to the Munich-Wistar rat, SNGFR is lower in the rabbit. This reflects the substantially lower glomerular ultrafiltration pressure in the rabbit, although this was offset partially by a higher Kf.

Animals↗
PubMed1991

Two types of sympathetic axon innervating the juxtaglomerular arterioles of the rabbit and rat kidney differ structurally from those supplying other arteries.

Ultrastructural analyses of serial thin sections have revealed two structurally different types of sympathetic axon innervating the afferent and efferent juxtaglomerular arterioles and the intralobular arteries in the outer cortex of the rabbit kidney. Both types of axon have also been found in association with an afferent arteriole in rat kidney. One axon type consists of relatively large diameter unmyelinated axons bearing varicosities in the form of slight expansions. The varicosities have a distinct structural zonation: synaptic vesicles occupy the expansion which faces the smooth muscle cells, whereas the rest of the axon is filled with numerous microtubules. The other axon type has varicosities containing vesicles and mitochondria but few microtubules. The varicosities are generally small and the intervaricosities very thin. The relationship of both axon types with support cells and/or basal lamina is sometimes poorly defined. Both axon types are catecholaminergic as their vesicles take up 6-hydroxydopamine and both types form junctions with arteriolar smooth muscle cells. As well as differing from each other, both types of intrarenal axon differ in several respects from those which innervate other arterial vessels.

Animals↗
PubMed1991

Significance of cardiovascular hypertrophy in the development and maintenance of hypertension.

The amplifier properties associated with the structural changes in the heart and resistance vessels in chronic hypertension together play a major role in maintaining the elevated blood pressure (BP) in chronic hypertension, which is greater than that of the initiating cause. In patients with primary hypertension, long-term antihypertensive drug therapy causes substantial regression of the structural changes, as assessed by normalization of the total peripheral resistance (including the nonautonomic component) and of the left ventricular (LV) mass. Reversal of LV hypertrophy (LVH) took considerably longer than reversal of the vascular changes and the more complete the reversal of LVH, the slower the rate of redevelopment of hypertension upon cessation of treatment. We observed no change in sympathetic activity or in renin-angiotensin-aldosterone levels during the redevelopment phase and we hypothesized that the cardiovascular amplifiers played a role in pathogenesis. This hypothesis was examined in spontaneously hypertensive rats (SHRs), where the vascular amplifier properties were developed substantially by 4 weeks of age, i.e., before the development of hypertension, whereas LVH occurred pari passu the rise in BP. When young SHRs were treated with enalapril for brief periods, there was almost complete long-term regression of vascular amplifier properties, but attenuation of LVH and hypertension were both smaller and more transient. In 4-week-old SHRs, complete abolition of sympathetic activity had a minimal effect on vascular amplifier properties, but affected LVH. Our findings suggest that LVH is as important in both the development and maintenance of hypertension as the structurally determined amplifier properties of the resistance vessels.

Animals↗
PubMed1991

Renovascular hypertension: information from experiments using conscious dogs.

1. Evidence from experiments in conscious, instrumented dogs shows that hypertension from renal artery stenosis is due to: (i) the stimulus, the mechanical resistance of the stenosis; and (ii) the secondary responses to this, especially angiotensin II (initially) and cardiovascular hypertrophy. 2. The hydraulic resistance of the stenosis is responsible for about 20-25% of the rise in blood pressure. 3. Angiotensin II is initially the most important secondary response to the stenosis. Within days, however, other as yet undetermined factors become dominant in the maintenance of the hypertension. The most important of these factors is probably cardiovascular hypertrophy. 4. These secondary factors are homeostatic, in that they mitigate the effects of stenosis on renal function.

Angiotensin II↗
PubMed1991

Evidence for a renomedullary vasodepressor system in rabbits and dogs.

Renal perfusion was increased in anesthetized rabbits and dogs by using an extracorporeal circuit. When left kidney perfusion pressure was raised in rabbits (145-240 mm Hg), arterial pressure fell by 1.34 +/- 0.20 mm Hg/min. Pretreatment of the rabbits with 2-bromoethylamine hydrobromide, which destroyed the renal medulla, abolished the fall in arterial pressure (-0.08 +/- 0.08 mm Hg/min) in response to increased renal perfusion pressure. In dogs (with blockade of autonomic ganglia by pentolinium, converting enzyme inhibition [captopril/enalaprilat], and surgical renal denervation), increasing renal perfusion pressure to 170-220 mm Hg resulted in a fall in arterial pressure by 0.32 +/- 0.03 mm Hg/min (or by 28.9 +/- 3.1 mm Hg over a 90-minute period). Mean arterial pressure did not change significantly in identically prepared dogs not subjected to increased renal perfusion pressure, whereas pretreatment of dogs with bromoethylamine abolished the hypotensive response to increased renal perfusion pressure. Thus, the hypotensive response to increased renal perfusion was dependent on the presence of an intact renal medulla, but hypotension still occurred in the presence of converting enzyme inhibition, autonomic ganglion blockade, and renal denervation. The results provide in vivo evidence in two species that a vasodepressor factor from the renal medulla is released in response to increased renal perfusion.

Animals↗
PubMed1990

Vascular actions of endothelin in the rabbit kidney.

1. The effect of two doses of endothelin, 10 and 50 ng/kg per min, i.v., on glomerular filtration rate (GFR), tubular stop flow pressure and pre- and post-glomerular vascular resistance have been studied in anaesthetized rabbits. 2. Blood pressure did not change significantly in response to 10 ng/kg per min endothelin or vehicle infusion, but rose steadily during infusion of 50 ng/kg per min endothelin, increasing 11.8 +/- 2.7 mmHg by 90 min of infusion. 3. Glomerular filtration fraction (3H-inulin extraction ratio) rose and remained elevated throughout the endothelin infusion at 50 ng/kg per min. GFR did not change significantly until 70-90 min of the infusion (50 ng/kg per min) when it decreased by about 35%. No significant changes were seen at 10 ng/kg per min endothelin. 4. Sodium excretion rate rose in response to the lower dose, due to an increase in fractional sodium excretion. No changes in sodium excretion were seen at the higher dose of endothelin. 5. Glomerular capillary pressure rose significantly in response to endothelin infusion (50 ng/kg per min). 6. Renal blood flow fell progressively in response to endothelin (50 ng/kg per min), to about one-third of the pre-infusion value. 7. Renal vascular resistance increased progressively with both doses of endothelin, by about 35% at 10 ng/kg per min and about 400% at 50 ng/kg per min after 70-90 min. Preglomerular resistance increased from 1.0 +/- 0.1 to 5.0 +/- 1.9 mmHg/mL per min in response to endothelin 50 ng/kg per min. Postglomerular resistance rose from 1.0 +/- 0.1 to 5.6 +/- 2.17 mmHg/mL per min. 8. Thus endothelin infusion caused progressive renal vasoconstriction with similar magnitude increases in both pre- and postglomerular vessels. The vasoconstriction of the kidney caused by endothelin occurred at a dose which did not effect systemic blood pressure.

Animals↗
PubMed1990

Atrial natriuretic peptide infusion causes vasoconstriction after autonomic blockade in conscious dogs.

Many studies have shown that atrial natriuretic peptide (ANP) reduces mean arterial pressure (MAP) in conscious animals by lowering cardiac output (CO) with no change or even increased total peripheral resistance (TPR). Because ANP is thought to be a vasodilator, the lack of fall in TPR in conscious animals is generally considered to be due to autonomic reflex increases in vascular resistance. In the present study in conscious, trained, chronically instrumented dogs (n = 7), we measured hemodynamic and renal excretory responses to 30-min infusions of alpha-human ANP (alpha hANP; 25, 50, and 100 ng.kg-1.min-1) in the presence and absence of autonomic nervous system blockade using the ganglion blocking agent pentolinium. In the absence of blockade, MAP and CO fell, whereas TPR rose with alpha hANP infusions, but these changes did not reach significance. There were significant increases in renal vascular resistance (RVR; 16-25%) and mesenteric vascular resistance (MVR; 14-40%). During autonomic nervous system blockade, alpha hANP caused dose-related reductions in MAP (7-12%), due to falls in CO (13-34%). Remarkably, the absence of autonomic reflex responses exposed substantial dose-related increases in TPR (5-33%). Autonomic blockade did not alter the ANP-induced increases in MVR but did abolish the rises in RVR. In summary, ANP caused vasoconstriction in mesenteric vasculature and substantial vasoconstriction in other nonrenal areas, independent of autonomic reflexes.

Animals↗
PubMed1990

Development of hypertension from unilateral renal artery stenosis in conscious dogs.

The renal and systemic changes after stenosis of the left renal artery (n = 5) or sham stenosis (n = 6) in conscious dogs were studied sequentially over 25 days. Stenosis produced a prompt rise in arterial pressure, which was at all times due to reduced peripheral vascular conductance, with no increase in cardiac output despite initial evidence of mild fluid retention. The decrease in peripheral conductance was attributable to 1) the stenotic kidney (25% of the total and due to the mechanical effect of the stenosis itself), 2) the nonstenotic kidney (about 15% of the total and not caused by angiotensin II), and 3) the nonrenal vasculature (60%). The decrease in conductance in the nonrenal vasculature was due partly to angiotensin II, but there was also a gradually developing non-angiotensin II component. Acute administration of captopril caused significantly greater changes in arterial pressure and peripheral conductance throughout the period of stenosis than before stenosis (and greater than in sham-stenosis dogs), indicating that angiotensin II was constricting the peripheral vasculature even when plasma renin levels were no longer elevated. In the stenotic kidneys, captopril produced a fall in renal vascular resistance, but renal blood flow did not rise because there was an approximately equal rise in the resistance of the stenosis. There was no evidence for a role for the autonomic nervous system in the hypertension, as ganglion blockade (pentolinium) had similar hemodynamic effects before and after stenosis. Thus, the hypertension was due at all times to reduced peripheral conductance, with the two kidneys responsible for 40% of this reduced conductance.

Animals↗
PubMed1990

Angiotensin II and the maintenance of GFR and renal blood flow during renal artery narrowing.

The time course of the renal blood flow and GFR responses to narrowing of the renal artery in conscious dogs is reviewed. The initial response to this threat to renal perfusion is renal vasodilatation, but within minutes a secondary vasoconstriction mediated by angiotensin II begins to develop. Angiotensin II-mediated contraction of mesangial cells is also demonstrable, but this does not apparently reduce the filtration surface area of the glomerular capillaries. The intrarenal effects of angiotensin II restore GFR back to normal within one to two weeks, by which time circulating plasma angiotensin II levels are no longer elevated. In contrast to its effects on GFR, angiotensin II has minimal effects on renal blood flow after stenosis. This may be because, (i) blood flow is mainly determined by the hydraulic resistance of the stenosis; (ii) renal vasoconstriction has relatively little effect on flow due to the particular hemodynamic properties of the stenoses, and (iii) a major site of action of angiotensin II may be within the glomerulus. Thus angiotensin II has a homeostatic role in the maintenance of GFR during renal artery narrowing and one component of this role may involve mesangial contraction.

Angiotensin II↗
PubMed1989

Renal venous wedge pressure in renal wrap hypertension in rabbits.

1. Renal cellophane wrapping to produce hypertension causes thickening of the capsule of the kidney. To determine whether this compresses the kidney, deep renal vein wedge pressure was measured as an estimate of tissue pressure in anaesthetized rabbits 1 month after cellophane wrapping (n = 5) or a sham operation (n = 3). 2. Renal vein wedge pressure was 18.3 +/- 2.0 mmHg in hypertensive rabbits and 8.4 +/- 1.1 mmHg in the sham-operated rabbits. 3. Arterial pressure was raised or lowered with angiotensin II or glyceryl trinitrate, respectively. Arterial and wedge pressures were approximately linearly related and, at any given arterial pressure, wedge pressure was approximately 8 mmHg higher in the cellophane-wrapped kidney than in the kidney of the sham-operated group. 4. These results, showing that renal wedge pressure is elevated in renal wrap rabbits, indicate that the kidneys are compressed, probably by the thickened renal capsule. This may explain the increased renal vascular resistance seen in this form of hypertension.

Angiotensin II↗
PubMed1989

Renal effects of atrial natriuretic peptide in conscious rabbits with renal wrap hypertension.

Atrial natriuretic peptide (ANP, 2 micrograms/min) was infused intravenously into rabbits four weeks after renal wrap or sham operation. Mean arterial pressure (MAP) averaged 132 +/- 4 mmHg in the renal wrapped rabbits and 89 +/- 3 mmHg in the sham rabbits, and glomerular filtration rate (GFR) was significantly lower in the hypertensive rabbits (6.2 +/- 1.0 ml/min) than in sham rabbits (8.9 +/- 0.7 ml/min). In sham rabbits, ANP caused a significant diuresis, natriuresis and increase in GFR. Enalapril pretreatment blunted these responses. In the hypertensive rabbits, ANP reduced mean arterial pressure but did not cause significant diuresis or natriuresis or change in GFR. Enalapril pretreatment did not significantly alter this response to ANP. In separate experiments, nitroprusside was infused to lower arterial pressure in hypertensive rabbits by a similar amount to that achieved with ANP and this reduced GFR, sodium and urine excretion rates. Thus ANP maintained GFR and sodium excretion in hypertensive rabbits compared to an equihypotensive dose of nitroprusside. In summary, ANP did not cause natriuresis or diuresis in renal wrapped kidneys at a dose which was effective in normal kidneys, but did maintain GFR, sodium and water excretion rates, compared to an equally hypotensive dose of nitroprusside.

Animals↗
PubMed1979

Sex offenders: three personality types.

Analyzed by a Q-type factor analysis MMPI profiles of 92 sex offenders institutionalized for psychiatric evaluation, which yielded three basic MMPI profile types. Altogether 88 of the 92 Ss coult be categorized into one of three types characterized by profile peaks on F,Sc; Pd,MA; or D,PD. Analysis of background information, social history items, nature of present crime, primary diagnosis, and ward observations revealed significant differences among the types. Of particular interest was the finding that the primary diagnosis for 85% of the "F,Sc" MMPI type was "no mental disorder" in spite of the fact that this group showed significantly more disturbed behavior on the ward (anxiety, depression, suspicion, and manic excitement) and had uniquely degraded their victims. The fact that two-thirds of these persons who had F scores greater than or equal to 80 and 50% denied the crime may have inadvertently affected diagnostic decisions.

Adult↗
PubMed1979

Acute renal haemodynamic and renin-angiotensin system responses to graded renal artery stenosis in the dog.

1. The acute renal haemodynamic and renin-angiotensin system responses to graded renal artery stenosis were studied in chronically instrumented, unanaesthetized dogs. 2. Stenosis was induced over 30 sec by inflation of a cuff around the renal artery to lower distal pressure to 60, 40 or 20 mmHg, with stenosis maintained for 1 hr. This resulted in an immediate fall in renal vascular resistance, but over the next 5--30 min both resistance and renal artery pressure were restored back towards prestenosis values. Only transient increases in systemic arterial blood pressure and plasma renin and angiotensin levels were seen with the two milder stenoses. Despite restoration of renal artery pressure, renal blood flow remained reduced at all grades of stenosis. 3. Pre-treatment with angiotensin I converting enzyme inhibitor or sarosine1, isoleucone8 angiotensin II greatly attenuated or abolished the restoration of renal artery pressure and renal vascular resistance after stenosis, and plasma renin and angiotensin II levels remained high. Renal dilatation was indefinitely maintained, but the normal restoration of resistance and pressure could be simulated by infusing angiotensin II into the renal artery. 4. The effective resistance to blood flow by the stenosis did not remain constant but varied with changes in the renal vascular resistance.

Angiotensin II↗
PubMed1978

The role of vasopressin in blood pressure control and in experimental hypertension.

1. The role of vasopressin in blood pressure control and in the pathogenesis of one-kidney Goldblatt hypertension in the conscious dog was investigated. 2. Infusion of synthetic arginine vasopressin to elevate plasma levels approximately five-fold caused bradycardia in normal dogs and increase in mean arterial blood pressure in dogs with pharmacological autonomic blockade. 3. A similar degree of elevation of plasma vasopressin concentration was observed after mild non-hypotensive haemorrhage. 4. Renal artery constriction in unilaterally-nephrectomized dogs caused a rise in plasma renin activity and only a doubling of plasma vasopressin concentration, but a marked rise in mean arterial blood pressure. 5. Vasopressin may play a role in normal cardiovascular homeostatic responses, but its role in the pathogenesis of this form of hypertension is unlikely to be significant.

Animals↗