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Austin Watson
Austin Watson

Buy Enalapril For Dogs


The clinical efficacy and safety of enalapril were evaluated in dogs with moderate or severe heart failure. This study was conducted at 19 centers and included 211 client-owned dogs with heart failure caused by mitral regurgitation (MR) due to acquired valvular disease or dilated cardiomyopathy (DCM). Dogs of various breeds, ages, and weights were included in the study. Replicates of 2 dogs each were formed, using separate allocation schedules for dogs with MR or DCM. One dog within each replicate received placebo tablets (vehicle tablets without enalapril) PO sid or bid, and the other dog received enalapril tablets at approximately 0.5 mg/kg sid or bid, based on individual need. In addition to the experimental drug, all dogs, except 1 in the placebo group, received furosemide; 73.3% of the dogs in the placebo group and 78.3% of those in the enalapril group received digoxin. Doses of enalapril or placebo were administered for approximately 28 days. In the placebo group, 68.6% of the dogs completed the study compared with 84.9% in the enalapril group; the difference between groups was significant (P




buy enalapril for dogs


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Objective: To determine whether the angiotensin converting enzyme inhibitor enalapril would lower systemic arterial and glomerular capillary pressure and reduce the magnitude of renal injury in a canine model of renal insufficiency.


Procedure: After surgical reduction of renal mass and baseline measurements, dogs in 2 equal groups received either placebo (group 1) or enalapril (0.5 mg/kg, PO, q 12 h; group 2) for 6 months.


Conclusions and clinical relevance: Data suggest that inhibition of angiotensin converting enzyme was effective in modulating progressive renal injury, which was associated with reduction of glomerular and systemic hypertension and proteinuria but not glomerular hypertrophy. Inhibition of angiotensin converting enzyme may be effective for modulating progression of renal disease in dogs.


Enalapril is used to treat heart conditions such as congestive heart failure, high blood pressure and valve disease in animals such as dogs and cats. It works by blocking the action of a substance in the body that can cause blood vessels to tighten and narrow, which helps to improve blood flow and reduce stress on the heart.


Spironolactone, an aldosterone antagonist with mild diuretic effects, substantially improves survival when added to standard cardiac therapy in humans with chronic CHF and low ejection fraction (14). Improved survival and reduction of risk for a cardiac event have recently been shown in dogs with DMVD and CHF (15). Amlodipine, a calcium channel blocker, has been shown in a pilot study to reduce the volume of MR, regurgitant orifice area, and left ventricle (LV) end-diastolic diameter in dogs, presumably by decreasing the systolic left ventricular pressure (16).


The current guidelines for the treatment of dogs with CHF secondary to chronic DMVD recommend the combination of drugs including at least furosemide, an ACEI, and pimodendan (17). Other drugs such as spironolactone and amlodipine may also be of benefit. However, the superiority of combination therapy over furosemide and pimobendan alone has not been documented.


The median survival time (MST) (from onset of CHF to death from all causes) was 430 d. The time to 75% survival was 99 d. At the end of the study 30.8% of these dogs were alive; therefore, the time to 25% survival could not be determined. The Kaplan-Meier survival plot is shown in Figure 1.


Kaplan-Meier plot of survival times (date of CHF diagnosis to date of death) in 21 dogs with CHF secondary to DMVD and treated with a combination of furosemide, ACEI, pimobendan, spironolactone, and amlodipine.


Spironolactone is mostly used for its antifibrotic effects via its aldosterone blocking action. In humans, RAAS inhibition by ACEIs becomes blunted after a while due to production of angiotensin II by alternate, non ACE-dependant mechanisms (14,34,35). This leads to increased aldosterone levels, mediating vasoconstriction and fibrosis. In the RALES study in humans, treatment with spironolactone was associated with a decrease in circulating levels of markers of fibrosis, and a 30% reduction in mortality compared with a placebo (14). A recent study showed that the administration of spironolactone at a dose of 2 mg/kg BW/d during a 14- to 15-month period significantly reduced the risk of morbidity/mortality by 55% compared with a placebo in dogs with CHF due to DMVD or DCM receiving conventional therapy (ACEI furosemide digoxin) (15). Note that the dose of spironolactone used in our dogs was lower (0.86 mg/kg BW/d).


Amlodipine is a calcium channel blocker, inducing arterial vasodilation, which can help to reduce the regurgitant fraction by reducing left ventricular pressure (16), in a similar fashion to hydralazine (40). Amlodipine could potentially activate the RAAS system, as shown in 1 study in which high doses were used (1.14 mg/kg BW/d). This effect was blunted by enalapril (41). In our study, lower doses were used (0.25 mg/kg BW/d) always in combination with an ACEI.


The principal limitation of this study is its retrospective nature. Therefore, biases could not be controlled as in a well-designed prospective study. In addition, the number of dogs included (21) is relatively low and only 11 (52%) dogs reached the defined endpoint of all-cause death, while 10 (48%) were censored since they were still alive at the end of the study. Censored cases weaken the power of the study The frequency of censoring in our study (48%) is similar to that reported in previous large prospective field studies conducted in dogs with ACEIs; 44% in LIVE (4) and 49% in BENCH (6) but is higher than the 25% reported in QUEST (13).


A total of 21 dogs and 11 event cases is low for survival analyses. Peduzzi et al (24) recommended not to exceed more than 1 variable per 10 subjects. Nevertheless, the data set was sufficient for 2 variables (initial daily dosage of furosemide and LA/Ao) to be identified as significantly negatively associated with survival in the multivariate analysis.


The endpoint for the survival analysis in our study was all-cause mortality. This is a robust endpoint that we consider the most clinically relevant. Previous large prospective field studies in dogs with heart failure (BENCH, COVE, LIVE, QUEST) used a combination of mortality plus treatment failure as the endpoint (3,4,6,13). Treatment failure is necessary as an endpoint in prospective studies for ethical and welfare reasons, but interpretation of results is problematic since treatment failure relies on subjective assessment by the clinician. For example, administration of concomitant treatments not allowed in the protocol is frequently used as an endpoint for treatment failure, and this is not the same as death or euthanasia.


Enalapril is a medication that is commonly used to treat high blood pressure (hypertension) and congestive heart failure in small animals. Enalapril can be given alone but is typically used in conjunction with other medications to treat congestive heart failure, especially when caused by degenerative mitral valve disease and dilated cardiomyopathy in dogs. Enalapril can also be used to treat patients with kidney failure or a disease that causes protein to leak into their urine.


Enalapril is only FDA approved for use in dogs (for treatment of mild, moderate, and severe heart failure) and is often used off-label in cats, ferrets, and birds. Veterinarians may also elect to prescribe the human version of this medication, under brand names that include Epaned and Vasotec, in an off-label capacity. The term off- or extra- label use means that a medication is used in a way, or in a particular species, that is not specified on the medication label. While veterinarians often prescribe medications for off-label uses, your veterinarian will determine whether this medication is right for your pet.


Follow the directions on the drug label or as provided by your veterinarian. This medication is typically given once or twice daily in dogs and cats, every 24 to 48 hours in ferrets, or every 8 to 48 hours in birds.


Ward JL, Chou YY, Yuan L, Dorman KS, Mochel JP. Retrospective evaluation of a dose-dependent effect of angiotensin-converting enzyme inhibitors on long-term outcome in dogs with cardiac disease. J Vet Intern Med. 2021;35(5):2102-2111.


Zatelli A, Roura X, D'Ippolito P, Berlanda M, Zini E. The effect of renal diet in association with enalapril or benazepril on proteinuria in dogs with proteinuric chronic kidney disease. Open Vet J. 2016;6(2):121-127.


Increased urine protein excretion is the hallmark clinicopathologic abnormality in dogs with protein-losing nephropathies. After the exclusion of preglomerular and postglomerular causes of increased urine protein excretion, such as immunoglobulin-producing neoplasms, hemoglobinuria, renal tubular disease, and any cause of lower urinary tract inflammation (e.g. bacterial infections or urolithiasis), glomerular disease can be presumptively diagnosed if the urine protein:creatinine ratio (UPC) is persistently > 0.5.


Pharmacologic inhibition of the renin-angiotensin-aldosterone system delays the development of azotemia and prolongs the survival of both people and dogs with glomerulopathies.6-9 Treatment with antiproteinuric drugs is recommended when the UPC ratio is > 2.010; however, the preferred drug class, dosage, and monitoring scheme remain unclear. In this article, I summarize the published support for administering angiotensin-converting enzyme (ACE) inhibitors and angiotensin II-receptor blockers (ARBs) and suggest an evidence-based treatment protocol. 041b061a72


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