Blood pressure levels in different clinical conditions in dogs
The study analysed 122 diseased dogs, with the mean systolic arterial pressure (SAP) varying across different clinical conditions. The varying range of mean systolic arterial pressure (136 to 161 mm Hg) was recorded in different clinical conditions in dogs. Although mean systolic arterial pressure was varying as per the number of the cases of various clinical conditions. Hypertension (SAP ≥160 mm Hg) was observed in obese dogs, as well as in dogs with ocular conditions and diabetes mellitus. The results shown in Table 2.
The findings of our study revealed variations in mean systolic arterial pressure among dogs with different clinical conditions, underscoring a lack of comprehensive literature on disease-specific blood pressure regulation. This variability may stem from diverse pathophysiological mechanisms, including altered RAAS activity, vascular tone and fluid balance in conditions like renal disease, hyperlipidemia, hyperadrenocorticism and hypothyroidism. Endocrine imbalances, systemic inflammation, oxidative stress and progressive organ damage further contribute to these differences, alongside individual variations in compensatory responses.
Distribution of hypertension (SAP ≥160 mm Hg) in dogs in different clinical conditions
The distribution of hypertension (SAP ≥160 mm Hg) across various clinical conditions in dogs showed that hyper-tension was most commonly associated with renal affections (21.62%), followed by cardiac conditions (13.51%). These findings are illustrated in Table 3.
The findings coincide with
Ware et al. (2021), who reported that the prevalence of hypertension in dogs with renal disease varied widely, ranging from less than 20% to over 75%. Similarly,
Charitha et al. (2023) found that chronic kidney disease accounted for the highest percentage (53.16%) of cases associated with secondary hypertension.
Elliott and Brown (2020) explained that several factors, including activation of the renin-angiotensin-aldosterone system (RAAS), over-activity of renal afferent nerves, decreased renalase production and phosphate retention causing bone and mineral disturbances, contribute to increased vascular tone in chronic kidney disease. These factors, combined with changes in body fluid volume relative to vascular volume and heightened vascular tone, result in elevated blood pressure.
Target organ damage (TOD) by clinical conditions
A total of 29 dogs diagnosed with renal affections were classified based on the risk of target organ damage (TOD) according to the ACVIM hypertension guidelines. Among these, the majority of dogs (51.72%) were in the prehypertensive stage, followed by 24.14% in the normotensive stage, while the remaining cases were evenly distributed between the hypertensive (12.07%) and severe hypertensive (12.07%) stages. Out of 11 dogs affected with cardiac disorders, 36.36% were classified in the hypertensive stage. An equal proportion (27.27%) were categorized as normo-tensive and pre-hypertensive, while 9.09% of the cases were in the severe hypertensive stage with systolic arterial pressure (SAP) ≥180 mmHg. Among the 06 dogs with ocular affections, 50.00% were in the prehypertensive stage, followed by 33.33% in the hypertensive stage and 16.67% in the severe hypertensive stage. In dogs presenting with ascites (n=23), the majority (60.86%) were normotensive, while 26.08% were in the prehypertensive stage and 13.04% were hypertensive. Of the 11 dogs diagnosed with haemoprotozoan infections, 45.45% were normotensive, 36.36% were prehypertensive and 9.09% were equally distributed between the hypertensive and severe hypertensive stages. In the group of 13 dogs suffering from gastroenteritis, 38.46% were normotensive, while 30.77% each were in the prehypertensive and hypertensive stages. Notably, no cases were observed in the severe hypertensive stage. Among the 05 dogs with epistaxis, 40.00% were in the prehypertensive stage, 40.00% were hypertensive and no dogs exhibited severe hypertension. Out of 04 dogs with obesity, 50.00% were prehypertensive, while 25.00% each were hypertensive and severe hypertensive. The results are depicted in Table 4.
Our findings are in partial agreement with the observations of
Singla (2015), who categorized dogs based on the risk of target organ damage (TOD) associated with systemic hypertension.
Charitha et al. (2023) reported that, among 48 dogs presenting kidney damage as TOD, 12 were classified in the moderate TOD risk group (SBP: 160-179 mm Hg), while 36 were categorized in the high TOD risk group (SBP ≥180 mm Hg). Chronic renal failure is associated with various alterations in blood pressure regulation, including sodium retention, extracellular fluid volume expansion, activation of the renin-angiotensin-aldosterone system (RAAS), increased norepinephrine levels, heightened vascular responsiveness to nor-epinephrine, reduced activity of vasodilatory substances, increased cardiac output, elevated total peripheral vascular resistance and secondary hyperparathyroidism. The pathophysiology of hypertension in renal failure is likely multifactorial, involving complex interactions of these factors
(Bartges et al., 1996).
Similarly, our findings partially align with the results of
Charitha et al. (2023) regarding cardiac TOD. They observed that among 22 dogs with heart involvement as TOD, 05 were classified under the moderate risk group, while the remaining 17 were in the high-risk group.
Yamini et al. (2020) also carried out a study to evaluate the clinical, electrocardiographic, radiographic and echocardiographic changes in dogs suffering from pulmonary hypertension (PH) secondary to mitral valve disease (MVD). Their findings revealed that 15.5% of the dogs with MVD had mild PH, 8.7% showed moderate PH and 4.8% were affected by severe PH.
Mahendran et al. (2022) also stated that in early cardiac disease, such as hypertension, increased pressure causes heart wall stress, triggering the release of natriuretic peptides like BNP and ANP. These peptides help lower blood pressure by promoting vasodilation and fluid excretion. Their rise reflects the heart’s response to persistent high pressure and volume overload in hypertension. Structural and anatomical abnormalities in the cardiovascular system are well-established causes of hypertension. Elevated systolic arterial pressure is recognized as a significant risk factor for cardiovascular diseases, including left ventricular hypertrophy and heart failure, both of which may result from sustained hypertension.
In accordance with
LeBlanc et al. (2011), our findings corroborate the frequent association of ocular issues with systemic hypertension in dogs. LeBlanc
et al. emphasized the importance of systematic monitoring for ocular TOD in hypertensive dogs or those with related systemic conditions.
Charitha et al. (2023) reported that, among 32 dogs with hypertensive ocular effects, 07 were categorized in the moderate risk group and 25 in the high-risk group. Similarly,
Singla (2015) identified 05 cases of ocular abnormalities, including corneal opacity and blindness, linked to hypertension. Ocular involvement is a well-documented and easily detectable clinical consequence of systemic hypertension in dogs, necessitating prompt identification and management.
Our study supports the conclusions of
Singla (2015) concerning ascites in hypertensive dogs. Among 08 cases of ascites reported by Singla, 06 dogs exhibited systolic arterial pressure (SAP) values <150 mm Hg, corresponding to minimal risk, while 1 dog had SAP in the range of 160-179 mm Hg, indicating moderate risk. Another case had SAP ≥180 mm Hg, placing it in the severe risk category.
Buob et al. (2011) described the liver’s dual blood supply from the portal vein and hepatic artery, which mix in the hepatic sinusoids. Portal hypertension arises from increased resistance to portal blood flow, often due to structural liver abnormalities like cirrhosis. Elevated portal pressure and altered sinusoidal permeability drive fluid into the peritoneal cavity, causing ascites.
The findings of this study indicate a significant association between hypertension and canine hemoprotozoan diseases. These results are consistent with the observations of
Koma et al. (2005), who attributed hypertension in dogs with hemoprotozoan diseases to chronic anaemia caused by the etiological agents. Chronic anaemia induces a hyperdynamic cardiovascular response, characterized by increased cardiac output and blood flow, along with a compensatory reduction in vascular resistance. This decreased vascular resistance is primarily attributed to reduced blood viscosity due to lowered haematocrit levels. While these vascular adaptations aim to maintain adequate oxygen delivery, they may inadvertently contribute to hypertension.
Our observations concur with
Fishbein et al. (2020), who identified hypertension in dogs with gastroenteritis as a result of enhanced sympathetic activation, upregulation of the renin-angiotensin-aldosterone system (RAAS) and impaired blood pressure autoregulation. These mechanisms, along with dehydration and electrolyte imbalances, exacerbate vasoconstriction, oxidative stress and vascular damage, contributing to acute severe hypertension.
Patel and Mitsnefes (2005) similarly noted that gastrointestinal infections, such as bacterial diarrhoea and haemolytic uremic syndrome, can worsen renal injury and chronic hypertension.
This research substantiates the conclusions drawn by
Brown et al. (2007) and
Bala et al. (2021), who associated epistaxis in dogs with systemic hypertension-induced vascular abnormalities.
Bala et al. (2021) categorized cases into prehypertensive and hypertensive risk groups, while
Bissett et al. (2007) highlighted hypertension-driven vascular damage as a cause of epistaxis. Hypertension induces endothelial damage, increased vascular permeability and reduced elasticity, predisposing vessels to rupture. While hypertension is a key factor, secondary conditions like trauma, coagulopathies, or inflammation may complicate diagnosis. Chronic hypertension exacerbates vascular fragility, reinforcing its role in the pathogenesis of epistaxis.
The analysis parallels that of
Bala et al. (2021), who reported the prevalence of hypertension risk categories in overweight and obese dogs (BCS 4 and 5), with 23.08% at minimal risk, 15.38% at mild risk, 48.72% at moderate risk and 12.82% at severe risk.
Montoya et al. (2006) also emphasized the role of weight status as a key risk factor for secondary hypertension. Obesity contributes to hypertension through mechanisms such as increased sympathetic nervous system activity, RAAS activation, endothelial dysfunction and vascular remodelling. Early obesity is characterized by renal sodium retention and extracellular fluid expansion, resetting the kidney-fluid apparatus to a hypertensive state. Elevated renin, angiotensin II and aldosterone levels exacerbate vasoconstriction and fluid retention. Insulin resistance and systemic inflammation further impair vascular function by promoting arterial stiffness. Additionally, adipocyte-derived hormones like leptin and neuropeptides influence central nervous system pathways, driving sympathetic over activation and linking obesity to hypertension
(Kotsis et al., 2010).
In this study, two diabetic dogs were evaluated, of which one (50%) was classified as prehypertensive (SAP: 140-159 mm Hg) and one (50%) as hypertensive (SAP: 160-179 mm Hg). These findings are consistent with
Herring et al. (2014), who reported systolic hypertension in 55% of diabetic dogs and
Priyanka et al. (2018), who observed higher mean systolic arterial pressure in diabetic dogs compared to healthy controls, with a hypertension prevalence of 58.82%. Similarly,
Singla (2015) documented one diabetic dog in the mild risk category (SAP: 150-159 mm Hg) and one in the moderate risk category (SAP: 160-179 mm Hg), with no cases of severe hypertension (SAP ≥180 mm Hg).
Hypertension is frequently associated with diabetes due to various pathophysiological mechanisms, as noted by
Kour et al. (2020). Disturbed lipid metabolism in diabetes induces vascular stiffness and reduced compliance, impairing blood pressure regulation. Generalized glomerular hyperfiltration in diabetic nephropathy leads to increased renal sodium retention and extracellular fluid expansion, contributing to elevated systolic arterial pressure. Additionally, increased peripheral vascular resistance and vasculopathy, driven by chronic hyperglycaemia and oxidative stress, further promote hypertension. These vascular changes, coupled with inflammation and activation of the renin-angiotensin-aldosterone system, establish a pro-hypertensive state, highlighting the necessity for integrated management strategies for diabetic dogs.
Systolic arterial pressure according to the stages of renal failure
According to the IRIS (
International Renal Interest Society 2019) guidelines, chronic renal failure (CRF) in dogs is staged based on serum creatinine levels. In the present study, the mean systolic arterial pressure (SAP) increased with the progression of renal disease, with values of 146.90±3.04 mm Hg in stage 2, 156.00±14.34 mm Hg in stage 3 and 159.00±7.55 mm Hg in stage 4. Hypertension (SAP ≥160 mmHg) was observed in 8 dogs. The prevalence of hypertension was notably higher in stages 3 and 4, emphasizing its strong association with advanced renal dysfunction. These results are detailed in Table 5.
Our findings are consistent with
Mann (2013) who reported 30.7% and 36% prevalence of hypertension in stage 3 and stage 4 of renal failure cases, respectively. The mean SAP gradually increased with increasing stage.
Jacob et al. (2003) demonstrated that dogs with elevated systolic arterial pressure (≥160 mm Hg) are at an increased risk of uremic crises and mortality due to a more significant decline in renal function.
Syme (2011) indicates that in dogs with chronic kidney disease, impaired renal sodium excretion results in heightened salt sensitivity, contributing to the development and exacerbation of hypertension.
