Blood Pressure/Hypertension not dropping

[Such1943]

However, for people with a history of high A1C (presumably many on this forum), indapamide is probably better than chlorthalidone. because it controls BP just as well, but with less metabolic/electrolyte disturbance.

I’m going to look into indapamide. I just had recent blood work on Monday, and it looks like HCTZ might be contributing to low potassium levels, even though I am chugging electrolytes like it's going out of style. It may also be negatively influencing some lipid markers and insulin sensitivity (fasting glucose of 87 mg/dL, Reta is taking care of this for me). I reviewed the labs with Dr. AI. On TRT+ (200mg Test, 150mg Primo and 4UI HGH. Lol TRT+ mild AAS cycle). Blood work was done before cycle to dial in IGF-1 (1 week in, 7 months on just 180mg Test). I'll find out more when I get another blood panel in 6 weeks. 115/70 this morning.

 

[diogenes]

Indapamide has slightly less hypokalemia (low K) risk than HCTZ or chlorthalidone, but it's not a game changer. All three are thiazide or thiazide-like diuretics—they do essentially the same thing. So switching to an equivalent dose of indpamide won't raise your potassium by much.

How low is your potassium (K)? Your telmisartan should raise K, so the fact that it's still low is noteworthy.

If it's just a bit too low, you might consider switching to 1.25mg indapamide. Your K will probably go up a bit, and your BP will have better 24 hour control than on HCTZ.

But if your K is way too low, you might not tolerate thiazide diuretics well. There are a few options, among them:

• just lower the HCTZ to 12.5mg. Your BP wlll climb a bit, but you'll have a good deal more K and maybe less fasting glucose. This is the "good enough for government work" solution.
• add amiloride or triamterene to your HCTZ/indapamide/chlorthalidone/whatever. This increases K and adds some more BP control. It's esp common for older patients. But whether it's a good idea for you depends on your kidney numbers bla bla bla bla and you need to ask your doctor (actually)
• switch to a potassium sparing diuretic. Again, whether this is a good idea depends on specifics about your kidney function. You're presumably male, so don't let them feed you spironolactone: it can make your dick soft and your skin girlish—perish the thought.
• switch from diuretics to some other class of drug. There is a whole zoo of lesser known but perfectly servicable antihypertensive drug classes: beta blockers, alpha2 agonists, alpha1 blockers, renin inhibitors, you name it. Some of my faves include:
  • nebivolol (beta blocker). Unlike older beta blockers, it's metabolically alright, long acting, erection friendly, and doesn't make exercise much harder. Most of the shit people talk about beta blockers doesn't apply to nebivolol.
  • prazosin (a1 blocker). Works well, may help sleep (esp nightmares), may help overall mental chillness, very safe. Start with a super low dose or it'll make you dizzy.
  • guanfacine ER (a2 agonist). Works. Safe. Enhances your calm. Improves your attention span. Might make you tired.

 

[Such1943]

How low is your potassium (K)? Your telmisartan should raise K, so the fact that it's still low is noteworthy.

January 5th blood draw: Potassium: 3.3 mmol/L. Quest Diagnostics standard: 3.5–5.3 mmol/L. Just under, nothing crazy. I might cut my HCTZ in half and request Indapamide at my yearly check up. Numbers were 110/66 this morning.

 

[diogenes]

Oh yeah 3.3 isn't even that bad, and 110/66 is on the low side. Consider cutting HCTZ to 12.5.mg. That might cure your hypokalemia, but it's not certain to. I predict it'll keep your BP around 120/80 and your K around 3.5—still on the low side.

If your K stays low-normal, consider prescription potassium supplementation to target like 4.0. You aren't going to outrun this on orange juice and bananas.

 

[Peptidesearch]

Has your pcp looked into secondary causes of htn? (Renal artery stenosis, pheochromocytoma, etc.)

I think these should also be ruled out as well

Primary Aldosteronism is another one that doctors are checking for more frequently.

Primary aldosteronism: a common cause of resistant hypertension​

Primary aldosteronism: a common cause of resistant hypertension - PMC

pmc.ncbi.nlm.nih.gov

 

[Peptidesearch]

January 5th blood draw: Potassium: 3.3 mmol/L. Quest Diagnostics standard: 3.5–5.3 mmol/L. Just under, nothing crazy. I might cut my HCTZ in half and request Indapamide at my yearly check up. Numbers were 110/66 this morning.

When I had low potassium from HCTZ I ended up being diagnosed with Primary aldosteronism, low potassium can be one of the symptoms.

I told my PCP it was caused by the diruretic as it was normal before. They said it I should still be able to tolerate it. Most doctors don't screen for it under previous guidelines, the new 2025 guidelines are below.
I ended up on an adolsterone blocker with other bp meds and my BP is finally in low normal range.

From Google:
New guidelines, particularly from the 2025 AHA/ACC and Endocrine Society, strongly recommend screening all patients with resistant hypertension (RHTN) for Primary Aldosteronism (PA), regardless of potassium levels, because hypokalemia is often absent but PA is a common, treatable cause of RHTN, involving measuring aldosterone-to-renin ratio (ARR) and continuing most antihypertensives (except MRAs) during initial testing. The European Society of Cardiology also supports broader screening for PA in all hypertensive patients.

Key Changes & Recommendations

• Universal Screening for RHTN: Screen all RHTN patients for PA, even if potassium levels are normal, due to its high prevalence (up to one-third of RHTN patients) and potential for specific treatment.
• Broader Hypertension Screening: The Endocrine Society www.endocrine.org

 

[Slogger]

Primary Aldosteronism is another one that doctors are checking for more frequently.

Primary aldosteronism: a common cause of resistant hypertension​

Primary aldosteronism: a common cause of resistant hypertension - PMC

pmc.ncbi.nlm.nih.gov

This is a really interesting article. I had just contacted my naturopath the other day about helping me find a BP med that can actually help my genetic high BP so I'm going to send the article to her. Thanks for sharing!

 

[Peptidesearch]

This is a really interesting article. I had just contacted my naturopath the other day about helping me find a BP med that can actually help my genetic high BP so I'm going to send the article to her. Thanks for sharing!

Thanks! I always wondered how much of the genetic high BP could be caused by Primary Aldo.
I have this condition unfortunately which took forever to get diagnosed as most doctors think it only affects a very small part of the population.

There's a new hypertension drug called Baxdrostat about to be released in 2nd quarter 2026 that I'm super excited to try.

Baxdrostat Granted FDA Priority Review for Hard-to-Control Hypertension, Could Be First-In-Class Therapy​

The US Food and Drug Administration (FDA) has accepted AstraZeneca’s New Drug Application (NDA) for baxdrostat under Priority Review for the treatment of adults with hard-to-control hypertension, including treatment-resistant cases.

The company expects the Prescription Drug User Fee Act (PDUFA) date in the second quarter of 2026. If approved, baxdrostat could become the first aldosterone synthase inhibitor authorized for clinical use.1

https://www.patientcareonline.com/view/baxdrostat-granted-fda-priority-review-for-hard-to-control-hypertension-could-be-first-in-class-therapy

 

[diogenes]

I don't get it. What does it matter whether you stop the synthesis of aldosterone or block it at its receptor? It seems exactly analogous to the difference between ACEIs and ARBs: You can block the synthesis of angiotensin 2, or you can block it at its receptor, and either way, you get almost exactly the same side effects and benefits. The few differences are small, and mostly about kinetics and off target action.

We already have spironolactone and eplerenone, both of which work well, with well described side effects. Is there any mechanistic reason we should expect this new synthesis inhibitor to perform better? Like, is there some reason this would cause less hyperkalemia? I can't think of one.

As far as I can tell from my limited googling, the phase 3 trial didn't directly compare baxdrostat to BP-equivalent doses of MRA drugs. And until they do, I see no reason to presume it should be better.

I hate to be too cynical, but this seems more like a drug company play to juice exclusivity out of a mechanism already well addressed by generics. No?

 

[aRareUnicorn]

Reta is known to wash out sodium and cause dry mouth. Combined with appetite reduction… and bad things can happen… my sodium dropped to 125, so not as low as the other poster…
I only avoided disaster because of some Good Samaritan on Reddit explained to me how critical low sodium can be… I already felt terrible but didn’t think it was because of low sodium. I read a lot about the impact, lowered my Reta dose and the most important -limited the liquids… with the lower dose my appetite improved a little and this helped too. All labs are more normal now.
If you are on Reta please make sure to check your labs and keep an eye on sodium. Taking electrolytes didn’t do much for restoring the levels, however taken proactively may help prevent the loss…
As a side note, my BP has not changed since starting Reta 7 months ago. Same with lipid levels and only a minuscule change in A1C. I did lose 55lbs in this time…